A case of complete decapitation in suicidal hanging : the mechanism and condition of decapitation.

Complete decapitation due to suicide by hanging is rare. We report the case of a decapitated man who was found in the sea near an estuary. A polyethylene rope was tied to the handrail of the bridge across a strait near the site of the body. The rope was 12 mm in diameter and 19 m in length from the handrail. It ended with a slip knot noose, and skin and mustache-like hair fragments were attached to it. The decapitated head was not found. The deceased weighed 82 kg and was 152 cm long without the head. The autopsy revealed coarse abrasions and intramuscular hemorrhage around the severed edge. The third cervical spine was not fractured. We reviewed the literature and suggested the conditions of body weight, fall height, rope diameter, and number of rolls in cases of decapitation by hanging. We calculated the hanging decapitation index (HDI) as the fall height (m) multiplied by the body weight (kg), divided by the rope diameter (mm), divided by the number of rolls ; and discussed the differences between complete and incomplete decapitation cases. J. Med. Invest. 70 : 290-293, February, 2023.

A case of fatal multi-organ inflammation following COVID-19 vaccination.

A 14-year-old Japanese girl died unexpectedly 2 days after receiving the third dose of the BNT1262b2 mRNA COVID-19 vaccine. Autopsy findings showed congestive edema of the lungs, T-cell lymphocytic and macrophage infiltration in the lungs, pericardium, and myocardium of the left atria and left ventricle, liver, kidneys, stomach, duodenum, bladder, and diaphragm. Since there was no preceding infection, allergy, or drug toxicity exposure, the patient was diagnosed with post-vaccination pneumonia, myopericarditis, hepatitis, nephritis, gastroenteritis, cystitis, and myositis. Although neither type of inflammation is fatal by itself, arrhythmia is reported to be the most common cause of death in patients with atrial myopericarditis. In the present case, arrhythmia of atrial origin was assumed as the cause of cardiac failure and death. In sudden post-vaccination deaths, aggressive autopsy systemic search and histological examination involving extensive sectioning of the heart, including the atrium, are indispensable.

An infant autopsy case of bowel obstruction due to internal abdominal hernia.

Internal abdominal hernia, defined as protrusion of viscera through a defect of the mesentery, has been considered a rare clinical entity. Recent clinical reviews reported a wide range of onset age (from newborns to the elderly) and symptoms (from minimal abdominal symptoms to severe acute abdomen). Sudden and unexpected death due to internal abdominal hernia is rare in infants or toddlers, and only 4 autopsy cases had been reported previously. We report the case of a 3-month-old Japanese boy who unexpectedly died 4 h after first vomiting. Autopsy showed a wide bowel obstruction with necrosis through a congenital mesenteric defect. The larynx was filled with gastric content (milky white viscous muddy material). In the cross section of both lungs, the same material was found to be expressed from the bronchioles. We diagnosed the cause of death as asphyxiation by viscous milk/vomitus aspiration caused by bowel obstruction due to an internal abdominal hernia. In case of sudden and unexpected death of an infant, autopsy is crucial to determine the cause of death. During autopsy, it is helpful to determine the character and distribution of gastric and airway contents to confirm milk or vomitus aspiration.

Sudden cardiac death during first-time jogging.

With increased interest in fitness and health care, jogging has become more popular as an exercise to promote health. However, sudden cardiac death during sports or exercise has also been reported. Some apparently healthy elderly individuals take up sports for both recreation and health improvement based only on completion of a questionnaire, without undergoing medical evaluation. We report the case of a 66-year-old Japanese man who suddenly died of acute ischemic heart disease during first-time jogging. He collapsed an hour after starting. A trainer promptly started cardiopulmonary resuscitation. An automated external defibrillator (AED) was applied, and defibrillation was attempted once by bystanders. However, he remained in cardiopulmonary arrest until he reached the emergency department, where he was pronounced dead. The autopsy found concentric hypertrophy of the left ventricular wall without fibrosis or degeneration, atherosclerotic changes in the coronary arteries, and severe lung congestion. We diagnosed death from acute myocardial ischemia. We suspect that many healthy elderly individuals have provoked a heart attack by prematurely attempting moderate or vigorous exercise, as in this case. The elderly require comprehensive medical assessment before exercise can be started. Moreover, this case shows that an AED is not always helpful. J. Med. Invest. 64: 184-186, February, 2017.

Postmortem Diagnosis of Anorexia Nervosa: An Endocrinological and Immunohistochemical Approach.

A female in her 30s was found dead after a fire. She was severely emaciated and had been diagnosed with anorexia nervosa (AN) about 5 years ago, but had not been treated recently. Therefore, we investigated not only her cause of death but also her condition of AN. Some of her organs weighed less than normal although no clear lesions were observed. In the pituitary gland, the number of follicle-stimulating hormone-immunopositive cells was markedly decreased although a normal number of thyroid-stimulating hormone-positive cells were detected. A histological examination of the ovary suggested that she had been suffering from amenorrhea. The thyroid gland was atrophic, and marked variations in follicle size were observed. Because we could not obtain enough volume of her blood for endocrinological examinations, we tried to investigate her endocrinological condition by immunohistochemistry. Immunohistochemical staining detected decreased triiodothyronine immunoreactivity and normal thyroxine immunoreactivity. The adrenal glands were also atrophic. Based on these findings, it was considered that she had been suffering from AN at the time of her death. The autopsy and other findings revealed that she had died of burning with carbon monoxide intoxication. J. Med. Invest. 63: 305-309, August, 2016.

Immunohistochemical investigation of the coma blister and its pathogenesis.

The erythematous patches and vesicles that are observed in coma patients, usually from an overdose of medication, are known as coma blisters. However, it is unknown whether the degenerated sweat gland is a necrosis or apoptosis. We immunohistochemically examined such skin lesions to investigate the characteristics and pathogenesis of the coma blister. Skin lesions were obtained from a forensic autopsy case, a woman in her thirties, of caffeine intoxication. Those lesions were observed in the left femoral, the lower left thigh, and the right knee. Histologically, the skin lesions showed that the keratinocytes had necrosed and the epidermis was thin in some areas. Eccrine sweat gland degeneration was observed. Obvious inflammatory cell infiltrations were not detected. Immunohistochemically, we stained each skin lesion against CD3, CD8, CD45RO, cytokeratin, 70 kD heat shock protein, ubiquitin, 150 kD oxygen regulated protein, and caspase-cleaved keratin 18 neo-epitope M30. They were also stained with an in situ apoptosis detection kit. Degenerated sweat glands featured CD45RO and M30 immunoreactivity. Immunohistochemical staining for CD45RO, CK-L, and M30 might be useful to observe sweat gland degeneration in the coma blister. Therefore, the apoptosis might be related to coma blisters and sweat gland degenerations.

An autopsy case of rhabdomyolysis related to vegetamin and genetic analysis of the rhabdomyolysis-associated genes.

We report an autopsy case of a man who died 2 days after taking an overdose of vegetamin. The autopsy findings were as follows: the epidermis on the axillary fossa and the inguinal skin had become macerated. Skeletal muscle was discolored. Concentrations of urea nitrogen, creatinine and urine myoglobin were 1.95 g/day, 0.66 g/day and 1100 ng/mL, respectively. Immunohistochemically, myoglobin was strongly stained at the Bowman's capsule, and tubular lumen and epithelium. 8-OH-dG was strongly stained in renal tubular epithelium in which cell nuclei were strongly stained. ORP-150 was observed in intraglomerular cells and renal tubular epithelium. The concentrations of phenobarbital, promethazine and chlorpromazine ranged from therapeutic to toxic levels, from toxic to lethal levels and toxic level, respectively. His cause of death was considered to be vegetamin-induced rhabdomyolysis. In genetic analysis of this subject, there were two heterozygous silent mutations in the three hot-spot regions in the RYR1 gene. In the CPT II gene, the subject was found to be heterozygous for an amino acid substitution in exon 4, (1203)G>A causing a (368)Val>Ile amino acid substitution. There was no mutation in the VLCAD gene or CYP2C19 gene. The subject was heterozygous for CYP2D6*1 and CYP2D6*2.

Microglial and astrocytic changes in the striatum of methamphetamine abusers.

Little is known about the role of glial cells in the striatum of chronic methamphetamine (METH) users. In this study, we immunohistochemically examined glial reactions in the striatum of chronic METH users who did not abstain from METH use and died of drug intoxication. Human glucose transporter 5 (hGLUT), a useful marker of microglia, and CR3.43, a major histocompatibility complex class II antigen specific for reactive microglia, were immunostained. Glial fibrillary acidic protein (GFAP) and S100 Beta were used for astrocyte immunohistochemistry. We analyzed 12 chronic METH users and 13 control subjects, and detected a 200-240% increase in the number of hGLUT5-positive cells in chronic METH users (p<0.01). However, we did not detect any proliferation of CR3.43-positive cells. The number of GFAP-positive astrocytes increased, but this increase was not significant (p>0.05). Moreover, S100B-positive cell density between the two groups was not significant (p>0.05). This study demonstrates the absence of reactive gliosis in the striatum of chronic METH users who did not abstain for prolonged periods from METH use. The results suggest that chronic METH use by itself did not activate glial cells in humans and reactive gliosis may not be involved in the mechanism underlying the loss of control in drug intake, which is a characteristic feature of drug addiction.

An autopsy case of severe pleuritis induced by misinsertion of a nasogastric nourishment tube: diagnostic significance of multinucleated giant cells.

An 87-year-old female who had been hospitalized due to pneumonia was administered nourishment through a nasogastric tube. She collapsed as a result of dyspnea after the insertion of a new tube and administration of nourishment. Chest X-rays revealed that the tube was inserted into the left pleural cavity passing the trachea and left bronchi and that the nourishment pooled. In spite of immediate treatment including removal of the tube and insertion of a drain, she died 12 days later. Autopsy findings: Both the left pulmonary and parietal pleurae were thickened and covered with a dirty gray-yellowish moss-like paste. The left lower lobe was softened, and this region was suspected as the ruptured site of the pleura. Histological findings: A part of the thick pleura with inflammatory cells, including multinucleated giant cells, was positive-stained for anti alpha-lactalbumin antibody immunohistochemically. These giant cells are often observed in granulomatous inflammation against a foreign material. It was considered that those in the pleura had been induced by the nourishment, and that those in the pulmonary parenchyma had been affected by the insertion of the tube. The multinucleated giant cells clarified the cause of fatal pleuritis and pneumonia and the misinsertion of the tube.

Genetic analysis of ryanodine receptor 1 gene and carnitine palmitoyltransferase II gene: an autopsy case of neuroleptic malignant syndrome related to vegetamin.

We report an autopsy case of a man in his forties who died 2 days after taking an overdose of vegetamin. The autopsy findings were as follows: externally, the upper epidermis of some parts of the body had become loosened. The epidermis was easily detached from the dermis using the fingers. Viscous fluid adhered around the nose and mouth. The brain was edematous and weighed 1520 g. Skeletal muscle was discolored. The urine was a slightly red-tinged yellow. The organs showed congestion. Urine tests: urea nitrogen: 1.95 g/day; creatinine: 0.66 g/day; urine myoglobin: 1100 ng/mL. Blood level of drugs: phenobarbital: 38.2 microg/ml; promethazine: 2.22 microg/ml; chlorpromazine: 0.96 microg/ml. Immunohistochemistry identified myoglobin in the kidney. From these findings, his cause of death was considered to be vegetamin-induced neuroleptic malignant syndrome and rhabdomyolysis. Mutation of the ryanodine receptor 1 gene is associated with malignant hyperthermia. However, there was no mutation which causes amino acid substitution in the three hot-spot regions of the ryanodine receptor 1 gene. Partial deficiency of carnitine palmitoyltransferase II is the commonest cause of recurrent rhabdomyolysis in adults. The subject was found to be heterozygous for an amino acid exchange in exon 4, (1203)G-->A causing a (368)Val-->Ile amino acid substitution. It is necessary to examine other candidate gene mutations.

The peroxidative DNA damage and apoptosis in methamphetamine-treated rat brain.

In this study, we investigated methamphetamine (METH)- induced peroxidative DNA damage in various regions of the rat brain. We injected METH to rats following 2 protocols. For the single administration experiment (group I), 50 mg/kg (i. p.) of METH was administered to observe the acute influence of METH. For the repeated administration experiment (group II), 10 mg/kg/day (i. p.) of METH was injected for 5 days. Immunohistochemically, peroxidative damage DNA, 8-hydroxy-2'- deoxyguanosine (8-OH-dG) was observed, and in situ apoptosis was also observed. In group I, immunoreactivity of 8-OH-dG was only enhanced in neurons of the nucleus accumben of METH-treated rats. On in situ apoptosis detection, positive findings were also enhanced in all examined parts compared to those in the control, though there were no significant increases in 8-OH-dG-immunopositive neurons except in the nucleus accumben. In group II, the nucleus accumben also showed enhanced 8-OH-dG immunopositivity compared to that in the control. There was no significant difference in apoptosis between the control and METH groups. Based on our observations, it is considered that METH induces oxidative DNA damage in the brain, especially in the nucleus accumben. However, those DNA damage might be caused differently between acute and chronic administration.

Toluene inhalation induced neuronal damage in the spinal cord and changes of neurotrophic factors in rat.

We investigated the effects of toluene inhalation on neurons and neurotrophic factors in the spinal cord and the relationship between them. Male Wistar rats were exposed to toluene (1500ppm for 4h per day) for 7 days. To observe damage of the neurons in spinal cord with the toluene, expression of microtubule associated protein 2 (MAP2) and 70kDa heat shock protein (HSP70) in spinal cord were performed by immunohistochemistry. MAP2 was degraded and HSP70-immunoreactivity was enhanced in nerve cell bodies of the gray matter in toluene inhalation group. Immunoreactivity of glial fibrillary acidic protein (GFAP), a marker of astrocytes, was enhanced in the toluene-treated group. Furthermore, glial cell line-derived neurotrophic factor (GDNF)- and brain-derived neurotrophic factor (BDNF)-immunoreactivity in spinal cord were slightly decreased in the treated group. In addition, the concentrations of GDNF and BDNF in the spinal cord were determined using enzyme linked immunosorbent assay (ELISA). Concentration of GDNF was reduced significantly by toluene exposure. BDNF also reduced, but not significantly. The toluene inhalation caused the damage of the neuron in the spinal cord, which was accompanied by the decrease in the neurotrophic factors, such as BDNF and GDNF.

Immunohistochemical investigation of dopaminergic terminal markers and caspase-3 activation in the striatum of human methamphetamine users.

Methamphetamine (METH) has been shown to induce neurotoxicity. In a previous human study using quantitative Western blotting and radioligand binding assay, dopaminergic terminal marker deficits were induced in chronic METH users. In this study, we examined the suitability of the immunohistochemical detection of tyrosine hydroxylase (TH), dopamine transporter (DAT), and vesicular monoamine transporter-2 (VMAT2) levels, and caspase-3 activation in the striatum to diagnose METH abuse. Decreases in TH immunoreactivity in the nucleus accumbens and DAT in the nucleus accumbens and putamen were induced in METH users, whereas a significant difference of VMAT2 was not evident between METH and control groups. However, in the nucleus accumbens of two METH users, levels of VMAT2, a stable marker of striatal dopaminergic terminal integrity, were reduced remarkably. These findings might indicate that dopaminergic terminal degeneration is induced in the striatum of some METH abusers. On the other hand, we observed little caspase-3 activation, indicative of apoptosis, in the striatal neurons of chronic METH users. Overall, the findings of dopaminergic terminal markers were similar to those in the previous human study. Therefore, it is suggested that immunohistochemical techniques could be used to examine dopaminergic terminal marker levels and could also give useful information on chronic and/or lethal METH use in cases of METH-related death, where METH intoxication may not be toxicologically demonstrated.

Prevention of lethal hepatic injury in Long-Evans Cinnamon (LEC) rats by D-galactosamine hydrochloride.

Repeated injections of D-galactosamine hydrochloride (GalN) increase the survival rate of Long-Evans Cinnamon (LEC) rats, an animal model of Wilson's disease. The aim of the present study was to investigate the mechanism of GalN for prevention of spontaneous lethal hepatic injury in LEC rats. Male LEC rats were given a single subcutaneous injection of 300 mg/kg of GalN or vehicle (0.9% NaCl) at 14 weeks, and killed at 28 weeks of age. Next, 6-week-old male LEC rats were given weekly subcutaneous injections of 300 mg/kg of GalN or vehicle for 3 or 12 weeks, and their hepatic 8-hydroxydeoxy-2'-guanosine (8-OHdG), glutathione peroxidase (GPX), and catalase activities were measured. None of GalN-treated rats died of hepatic injury (0/12), whereas the mortality rate of control rats given 0.9% NaCl was 17% (2/12). GalN administration for 12 weeks decreased the hepatic 8-OHdG, and GalN administration for either 3 or 12 weeks increased the glutathione peroxidase activity. GalN administration increased the serum level of alanine aminotransferase, and accelerated megalocytic degeneration of the hepatocytes. GalN treatment is effective in preventing lethal hepatitis in LEC rats and decrease of oxidative DNA damage by GalN plays an important role in increase of the survival rate.

An autopsy case of adrenal insufficiency 20 years after hypophysectomy: relation between stress and cause of death.

A 63-years-old man was found dead with the body soaking in water lying face up on a riverbank. Autopsy and diatom examination demonstrated that the cause of death was drowning. He had undergone hypophysectomy 20 years earlier. Autopsy, pathological and endocrinological findings demonstrated secondary and chronic hypothyroidism, hypogonadism, and adrenal insufficiency. The cadaver had fallen into the river, and received numerous wounds such as abrasions and subcutaneous hemorrhage. Moreover, it was suspected that he had developed hypothermia before death. Cortisol in the blood and 17- OHCS in urine were within the reference range. We suspect that the adrenocortical hormone was secreted into the blood as a result of various stresses due to wounds and hypothermia. However, it was suspected that sufficient hormone might not be secreted due to chronic adrenal insufficiency. This insufficient cortisol causes the decrease in the stress resistance, and might influence his cause of death. Moreover, as hypothyroidism decreases thermogenesis, he might have fallen into hypothermia easily. In addition, because both adrenocortical insufficiency and hypothyroidism caused the hypoglycemia, he might have fallen into the loss of consciousness. Therefore, it was considered that he had died by drowning, in relation to the adrenocortical insufficiency and panhypopituitarism.

Changes in renal function and oxidative damage in methamphetamine-treated rat.

In this study, we observed renal damage and peroxidative injury as the acute or sub-acute effect of methamphetamine (MA) to determine whether MA intoxication can be diagnosed from immunohistochemical changes in the kidney. In addition, renal function was investigated in relation to the immunohistochemical changes. A single administration of MA (group I) (50mg/kg/ (i.p.)) and repeated administration (group II) (10mg/kg/day (i.p.) for 5 days) were designed as an acute model and a sub-acute or chronic model. Immunohistochemically, cell damage markers were observed. Then, renal function markers and minerals in blood were measured. Myoglobin and creatinine phosphokinase (CPK) in blood were also analyzed. In group I, ubiquitin immunoreactivity was enhanced only in the renal tubules. Creatinine increased, while K, Ca, and P decreased (P<0.01). CPK increased significantly (P<0.01). Therefore, it was suspected that MA might induce renal dysfunction with renal tubule damage. This damage might be related to leakage of CPK from muscle. In group II, 8-hydroxy-2'-deoxyguanosine (8-OH-dG) increased immunohistochemically and quantitatively (P<0.01). It was considered that oxidative DNA damage might be induced by repeated administration. It was considered that this study offers basic information for the evaluation of pathological changes in the kidney in MA-related autopsy cases.

Effect of hypothermia on postmortem alterations in MAP2 immunostaining in the human hippocampus.

Ischemic neuronal injury induce degradation of microtubule-associated protein 2 (MAP2). In addition to ischemia, postmortem brains show alterations in MAP2 immunoreactivity in the hippocampus, suggesting that the factors inducing cytoskeletal disruption in postmortem brain are similar to those in ischemic brains. Hypothermia reduces the severity of ischemic injury including disruption of MAP2 in the hippocampus. However, whether hypothermia reduces postmortem changes of MAP2 was not clear. In this study, we evaluated the effect of hypothermia on postmortem degradation of MAP2 in the human hippocampus at various postmortem intervals using immunohistochemistry. In postmortem brains without hypothermia (the normothermic group), the locus of MAP2 immunoreactivity moved from the dendrites to the cell bodies prior to becoming undetectable with increasing postmortem interval, particularly in the CA1-subiculum region. On the other hand, the change in MAP2 immunoreactivity was remarkably attenuated in brains of death from cold (the hypothermic group). The present study demonstrated that MAP2 disruption is remarkable in the CA1-subiculum region of autopsied brains and that hypothermia reduces the postmortem change of MAP2, as observed in ischemic brain. Therefore, immunostaining of MAP2 in the hippocampus could be used to diagnose hypothermia.

Toluene inhalation-induced adrenocortical hypertrophy and endocrinological changes in rat.

Rats were exposed to toluene (1,500 ppm for 4 hr per day) for 7 days. The body weight of the rats was significantly lower and the weight of the adrenal gland was significantly higher in the toluene inhalation group compared to the controls. Microscopically, there was no obvious change in the medulla, but hypertrophy of the cortex was observed in the toluene inhalation group. And, the size of adrenocortical cells in treated-rats was also significantly enlarged than the control. Immunohistochemical staining did not show a clear difference in localization of aldosterone-positive cells between the control and inhalation groups. Expansion of the corticosterone-positive area consistent with the cortical hypertrophy was recognized in the inhalation group. Enhancement of 72 kD-heat-shock protein (HSP70)-expression in the toluene inhalation group was not observed. Neither stress nor damage to cortical cells due directly to toluene exposure was observed in the cortex. Also, there was no obvious difference in the anti-proliferating cell nucleus antigen (PCNA)-immunostaining between control and inhalation groups. Thus, it is suspected that cortical hypertrophy was the result of cell enlargement due to the stimulation of the cortical cells. Corticotropin-releasing factor (CRF) immunoreactivity in the paraventricular nucleus (PVN) was increased in the inhalation group. Concentration of plasma ACTH was elevated significantly by toluene exposure. The amounts of mRNA of adrenocortical steroid metabolism gene, cytochrome side-chain cleavage (P450scc), was also increased by toluene inhalation. Toluene exposure might induce adrenocortical hypertrophy via the hypothalamus-pituitary-adrenal gland (HPA) axis.

Effect of hypothermia on postmortem alterations in MAP2 immunostaining in the human hippocampus.

Ischemic neuronal injury induce degradation of microtubule-associated protein 2 (MAP2). In addition to ischemia, postmortem brains show alterations in MAP2 immunoreactivity in the hippocampus, suggesting that the factors inducing cytoskeletal disruption in postmortem brain are similar to those in ischemic brains. Hypothermia reduces the severity of ischemic injury including disruption of MAP2 in the hippocampus. However, whether hypothermia reduces postmortem changes of MAP2 was not clear. In this study, we evaluated the effect of hypothermia on postmortem degradation of MAP2 in the human hippocampus at various postmortem intervals using immunohistochemistry. In postmortem brains without hypothermia (the normothermic group), the locus of MAP2 immunoreactivity moved from the dendrites to the cell bodies prior to becoming undetectable with increasing postmortem interval, particularly in the CA1-subiculum region. On the other hand, the change in MAP2 immunoreactivity was remarkably attenuated in brains of death from cold (the hypothermic group). The present study demonstrated that MAP2 disruption is remarkable in the CA1-subiculum region of autopsied brains and that hypothermia reduces the postmortem change of MAP2, as observed in ischemic brain. Therefore, immunostaining of MAP2 in the hippocampus could be used to diagnose hypothermia.