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Our research groups have studied the movement and injury characteristics of the human body in a side collision between the front of a small car and a pedestrian. This study discusses the movement and injury characteristics of the human body in a side collision between the front of a small car and bicycle.A total of 31 cases of traffic accidents caused by small car collisions when riding a bicycle across a road were collected. Through on-site inspection and trace inspection of the accident vehicles and bicycles, the speed of the car during the collision was calculated, the collision relationship between the small car and bicycle was determined, and the injury site and degree were determined through autopsy. The car speed was divided into two groups:60 km/h and60 km/h. Injuries of the skull, cervical spine, ribs, pelvis, femur and tibiofibular were analysed, and the correlations with the height of the bicycle controller, the height of the bicycle seat, the height of the car hood and the length of hood were discussed. PC-Crash was used for simulation analysis to further clarify the injury process.The ratio of the height of the bicycle seat to the height of the hood plus the length of the hood in the windshield-damaged group was larger than that in the undamaged windshield group (P 0.05). No cervical fracture was found when V 60 km/h, and 52.94% of cases had cervical fracture when V 60 km/h. The ratio of the height of the bicycle seat to the height of the hood in the pelvic fracture group was smaller than that in the nonpelvic fracture group (P 0.05). The incidence of tibiofibular fracture was less than 65%.When a side impact between a car front and a bicycle occurs, the resulting human injury is related not only to the speed but also to the height of the bicycle seat and the height and length of the hood of the car. The incidence of tibiofibular fractures was significantly lower than that of small car front-pedestrian side impacts.

The patient was an 88-year-old woman with a 10-year history of hypertension. She was suspected to have been hit by a car. At the time of the event, she was conscious and able to stand on her own and had no obvious injuries. She was sent home, but she lapsed into unconsciousness and was nonresponsive after 2 hours. She was sent to the hospital, and her heartbeat and breathing stopped. After half an hour of rescue attempts, her heartbeat did not recover, and she was declared dead. During the autopsy, a small subcutaneous hemorrhage was observed below the right knee joint. No obvious internal organ injuries or bone fractures were observed. The deceased also had mild atherosclerosis in the coronary arteries and an old cerebral infarction in the right cerebellum. The tissue histopathological tests showed distinct fat embolism in multiple organs, including the brain, lungs, kidneys, liver, and pancreas. A postmortem blood biochemistry test of the heart blood showed that the levels of low-density lipoprotein, cholesterol, triglycerides, and free fatty acids in the blood were increased, and the level of C-reactive protein was elevated. According to the autopsy results, the direct cause of death was multiorgan fat embolism. This case suggests that aging, hypertension, and hyperlipidemia may be risk factors for nontraumatic fat embolism under stressful conditions.

OBJECTIVE To discuss the collision relationship and the cause of the fracture caused by traffic accidents in which the front of a small car collides with the side of a pedestrian while braking. METHODS The surveillance videos of 42 traffic accidents involving the front of a small car colliding with the side of a pedestrian while braking were collected. By analyzing the surveillance videos and the paths, the speed of the collision, the relationship between the vehicle and the pedestrian upon collision, and the movement trajectory of the human body were clearly identified. The type and severity of the injuries were also determined through autopsy. The characteristics of the human injuries and vehicle paths were analyzed according to the collision speed (

Transverse fracture of the skull base is common both in the crushing of temporal regions of the skull and in the case of force acting on one temporal region. However, the mechanism of transverse skull base fracture caused by maxillofacial force has not been fully clarified. To provide an injury identification basis for forensic pathologists and clinicians, this paper combines accident reconstruction and finite element analysis methods to study the injury mechanism of an incomplete transverse fracture of skull base after the injured individual’s mandible was subjected to violence in a traffic accident. The results show that after the injured individual’s mandible was subjected to violence, forces in the direction of the left mandibular fossa and the right mandibular fossa were generated, creating the component forces. The combination of the two forces can produce a crushing effect toward the center of the skull base, as if the left and right temporal regions are being crushed, and the stress is concentrated at the joint of the mandible, the middle cranial fossa and the hypophyseal fossa. When the stress exceeds a certain limit, it will cause a transverse fracture of the skull base.

BACKGROUND Karoshi, which is sudden death associated with overwork, has become a serious problem in China. Many studies have examined the relationship between cardiovascular risks and karoshi, but there is little evidence that explains the exact mechanism by which overwork induces sudden death. In these cases, there are few obvious positive findings from forensic autopsies except for histories of overwork prior to death. Therefore, we assume that abnormalities, such as cardiac arrhythmia, rather than organic changes are the cause of karoshi. MATERIAL AND METHODS In the present study, the forced swim test (FST) was used to establish models of overwork. The myocardial tissues of SD rats taking FST (1 h per day, for 30 consecutive days) were collected. The arrhythmia-related molecule CX43 as well as its upstream regulation molecule Cav-1 and cSrc were tested by Western blot (WB) and immunohistochemistry (IHC). HE staining and Masson's staining were performed in the myocardium tissue section. RESULTS We observed downregulation of caveolin-1 (Cav1) followed by cSrc activation, resulting in the decrease of connexin43 (Cx43) levels in overwork models. Myocardial interstitial fibrosis, which is associated with electrophysiological aberrances that result in arrhythmia, was also found in the overwork models. CONCLUSIONS These data provide a mechanistic explanation for the speculated link between karoshi and cardiac arrhythmias.

Karoshi is a term used to describe unexplained sudden death associated with overwork and has become a serious public health issue in China. Cases have occurred in physicians, university professors, engineers in high-tech companies, and blue-collar workers. The mechanisms associated with death by overwork are very complex. According to most researchers, karoshi is considered to be caused by an excessive workload that induces deterioration of underlying hypertension or atherosclerosis. These conditions inevitably lead to death from cardiovascular or cerebrovascular diseases. However, in our own experience, we have found that in some cases, the victims of karoshi were in a chronic state of overwork but without a history of cardiovascular or cerebrovascular diseases. In support of this, we have found that even autopsies have revealed few positive findings except for cardiac hypertrophy. In this article, we report 3 typical cases of karoshi but without the typical pathomorphological features of cardiovascular or cerebrovascular disease.

This report describes a case of blunt cardiac injury and pericardial tamponade after video-assisted thoracoscopic surgery in a patient with lung cancer, hypertension, and cardiac hypertrophy. Anatomic findings included massive hemorrhage in the pericardium, cardiac hypertrophy, and a superficial contusion with a ruptured blood vessel on the epicardium at the lateral wall of the left ventricle. The patient died of pericardial tamponade secondary to blunt trauma from the tip of the thoracoscopic instrument. This case suggests that detailed assessment of the cardiovascular system, especially cardiac hypertrophy, careful preoperative preparation, and careful monitoring of postoperative conditions are important.

A full-term female baby born to parents who gave birth three years prior to a girl who survived only 31h postpartum died 36h after birth. An autopsy showed that the heart was markedly hypertrophic (32g). Microscopically, the myocardium, liver and kidney cells exhibited extensive vacuolar degeneration. Sudan III staining was positive in cardiac muscle, liver and kidney tissue. Tandem mass spectrometry analysis revealed that the deceased patient had a carnitine palmitoyl transferase II (CPT2) deficiency or a carnitine-acylcarnitine translocase deficiency. Genetic testing of the parents revealed heterozygous CPT2 mutations, indicating that their offspring would have a 25% chance of having a CPT2 deficiency. Therefore, we speculated that CPT2 deficiency might be the cause of death based on the results of staining, tandem mass spectrometry analysis and parental genetic testing.

BACKGROUND Sudden death from ischemic heart disease while driving is an important cause of traffic accidents. This study discusses causes of traffic accidents in relation to risk factors for acute myocardial infarction such as hypertension and overwork and provides references for the early prevention and regulation of drivers' health conditions. MATERIAL AND METHODS Data on 21 cases of sudden death by ischemic heart disease while driving from January 2015 to December 2019 were collected. Age, symptoms, and cardiac pathological changes of patients were summarized by systematic anatomical and medical history data. RESULTS Patients were 21 men with an average age of 47±7.27 years (most aged 40 to 60 years), and the average weight of their hearts was 439.45±76.3 g. Twelve patients had a history of hypertension, 8 had previous myocardial infarction, and 4 had fatty liver. All had at least 1 severe narrowing of a major coronary artery. Twelve patients died within a short period; 9 died more than 12 h after myocardial infarction onset. Ten patients had worked more than 80 h of overtime per month, 4 patients, more than 45 h, and 7 patients, less than 45 h. CONCLUSIONS Regular physical examination and information about ischemic heart disease should be emphasized for men aged 40 to 60 years who drive frequently, especially for those with hypertension, overwork, or previous myocardial infarction. Incorporating objective evaluation criteria for the severity of ischemic heart disease and overwork into health condition-related driving regulations is needed.

Sudden cardiac death (SCD) is the most frequent cause of sudden unexplained death in forensic practice. The most common cause of SCD is coronary artery disease related to coronary atherosclerosis. Previous study suggested the possible application of connexin 43 (Cx43) and zonula occludens-1 (ZO1) immunostaining in the early diagnosis of myocardial ischemia. However, there appears to be insufficient data with regard to their mRNA levels. The present study investigated the cardiac mRNA levels of Cx43 and ZO1, using forensic autopsy materials consisting of 41 control cases without any disease or structural abnormality of the heart (group 1), 32 deaths due to acute ischemic heart disease related to coronary atherosclerosis without apparent myocardial necrosis (group 2), and 29 traumatic deaths with coronary atherosclerosis (group 3). Ten candidate reference genes were evaluated in the left ventricles of 10 forensic autopsy cases. EEF1A1, PPIA, TPT1, and RPL13A were identified as the most stable reference genes. Using these validated reference genes, mRNA levels of Cx43 and ZO1 were examined in the bilateral ventricles and atria of the heart. Relative mRNA quantification demonstrated decreased calibrated normalized relative quantity (CNRQ) values of Cx43 and ZO1 in bilateral ventricles of group 2. When using one conventional reference gene (GAPDH or ACTB) for normalization, nearly no difference was detected among the three groups. These findings indicate that ventricular gap junction remodeling may be a key contributor to rhythm disturbances. Analysis of cardiac Cx43 and ZO1 using real-time PCR is useful in diagnosis of SCD, and validation of reference genes is crucial.

Tyre imprints on the skin are usually considered to be the result of being run over by a motor vehicle. This article reports a traffic accident in which tyre marks on the victim’s skin were caused by a collision rather than by being run over. The mechanism of the injury in this case is analysed and discussed. A 23-year-old male drove a motorcycle while under the influence of alcohol and collided with a sign pillar on the side of the road. Both the victim and the motorcycle careened into the bottom of a tractor-trailer. No witnesses or surveillance videos could confirm the process of the accident. Because tyre imprints were found on the victim’s skin, traffic police believed that he had been run over during the accident. However, forensic autopsy and analysis of the accident process revealed that the true cause of the imprints was a collision between the victim’s body and a tyre.

An elevated serum tryptase concentration is considered a specific marker for systemic mast cell activation, a central feature of anaphylaxis. However, in some cases of acute cardiovascular death, high concentrations of serum tryptase are also observed. We compared the postmortem serum tryptase concentrations in 74 cases assigned to the following four groups: anaphylactic deaths (Group A, n = 20), acute cardiac deaths (Group ACD, n = 30), acute dissecting aneurysm ruptures (Group ADA, n = 10), and controls (Group C, n = 14). Additionally, the cutoff between Group A and the other groups was calculated using receiver-operating characteristic (ROC) curve analysis. Tryptase concentrations were markedly elevated in Group A (p < 0.001), Group ACD (p = 0.015), and Group ADA (p = 0.005). The optimal cutoff was 43 ng/mL, the sensitivity was 90%, and the specificity was 98%. While elevated concentrations of tryptase were noted in practical autopsy cases, due attention should be paid to the differential diagnosis between anaphylactic and acute cardiovascular deaths.

The present study investigated the morphology of astrocytes in the hippocampus and serum S100B levels in cases of mechanical asphyxia due to neck compression (n=23: atypical hanging, n=7; ligature/manual strangulation, n=16) with regard to the classical autopsy findings, compared with those of other types of asphyxiation (n=9) and acute myocardial infarction/ischemia (AMI, n=20). The decrease in intact astrocyte number, as shown by S100 and GFAP-immunostaining, was larger for asphyxiation due to neck compression compared with that for other asphyxiation and AMI, showing a correlation with the increase in the serum S100B levels. The decrease in intact astrocyte number and increase in serum S100B were closely related to the severity of conjunctival petechial hemorrhage and fracture(s) of the hyoid bone and/or thyroid cartilage in asphyxia due to neck compression. These findings suggest that hippocampal astrocyte injury is caused by cerebral hypoxia accompanied by congestion, especially in mechanical asphyxia due to neck compression.

It is difficult to examine the intact in situ status of thoracic organs, including the heart and lungs, after opening the chest at autopsy. The present study investigated the pathological diagnostic significance of the cardiothoracic ratio (CTR) with regard to heart and lung weight in postmortem plain chest radiography. The pathological diagnostic significance of the CTR in postmortem plain chest radiography using serial forensic autopsy cases of adults (>19 years of age, n=367, within 72 h postmortem) was retrospectively investigated. In natural deaths, CTR was larger for heart diseases, and was smaller for pulmonary infection and gastrointestinal bleeding, showing correlations to the heart weight except in cases of hemopericardium. In traumatic deaths, CTR was larger in cases of fire fatality and acute methamphetamine intoxication, and varied in cases of blunt injury, showing correlations to the heart weight. However, CTR was smaller for sharp instrument injury and drowning, independently of the heart weight. These findings suggest that postmortem CTR (median, 55.6%, measured using a mobile X-ray apparatus) primarily depends on the heart weight, but is substantially modified during the process of death: the CTR may be enlarged by cardiac dilatation due to terminal congestive heart failure, but may be reduced by inflated lungs in drowning or hypovolemia due to fatal hemorrhage. CTR showed a mild correlation to the right diaphragm level, which was also related to the cause of death, but was independent of the left diaphragm level. Plain chest radiographic findings may also be helpful in investigating the pathophysiology of death, and are to some extent comparable with clinical findings. This also suggests the potential usefulness of postmortem CT and MRI for analysis of terminal cardiac function.

The clinical features suggest that genetic factors may have a strong influence on susceptibility to coronary artery disease (CAD). The aim of this study was to investigate the association between FokI (rs2228570) and BsmI (rs1544410) of the vitamin D receptor (VDR) gene polymorphisms and patients with CAD in a Chinese population. One hundred and fifty-two CAD patients and 212 healthy controls were genotyped for the FokI and BsmI polymorphisms in VDR gene using polymerase chain reaction-restriction fragment length polymorphism. No significant differences were observed in the genotype and allele frequencies of the FokI and BsmI polymorphisms between the cases and controls (For FokI: odds ratio = 1.11, 95% confidence interval 0.83-1.50; for BsmI: odds ratio = 0.74, 95% confidence interval 0.44-1.23). There was no significant difference in the genotype distribution or the allele frequencies of VDR FokI and BsmI between two groups in a Chinese population.

To investigate hematological and serum protein profiles of cadaveric heart blood with regard to the cause of death, serial forensic autopsy cases (n = 308, >18 years of age, within 48 h postmortem) were examined. Red blood cells (Rbc), hemoglobin (Hb), platelets (Plt), white blood cells (Wbc), total protein (TP) and albumin (Alb) were examined in bilateral cardiac blood. Blood cell counts, collected after turning the bodies at autopsy, approximated to the clinical values. Postmortem changes were not significant for these markers. In non-head blunt injury cases, Rbc counts, Hb, TP and Alb levels in bilateral cardiac blood were lower in subacute deaths (survival time, 1–12 h) than in acute deaths (survival time

The victim (59-year-old male) used a long hemp rope tied between his neck and a cherry tree while attempting to drive his car away, resulting in complete decapitation. At autopsy, the decapitation wound of the head and the torso corresponded perfectly; a clear-cut severance plane was found at the bottom of the skull. In contrast to suicidal decapitation by hanging and traumatic railway injury, autopsy findings for vehicle-assisted ligature strangulation are rarely reported. A review of the literature concerning suicidal vehicle-assisted ligature strangulation suggested a striking young or adult male predominance, and the wound margins were usually clear-cut with a sharply-demarcated encircling abrasion zone. The present case presented some notable autopsy findings involving wound morphology and pathological changes in organs related to the mechanisms of injury and death. Despite complete decapitation, the face was congestive, the lungs were congested with findings of acute respiratory distress, and the brain was markedly swollen with diffuse and severe astrocyte injury, suggesting that asphyxiation was involved in the death before decapitation.

Adrenocorticotropic hormone (ACTH) is involved in systemic reactions to stress. The aim of the present study was a comprehensive analysis of serum and cerebrospinal fluid (CSF) levels of ACTH, and the pituitary immunohistochemistry with special regard to fatal hypothermia in routine forensic autopsy cases (n=162: 5-97 years of age; 114 males and 48 females; 4 h to 3 days postmortem, median, 19.2 h). The ACTH concentrations were independent of the postmortem time, gender, or age of the subjects. The serum ACTH level was similar to the clinical reference value for sharp instrument injury, fire fatality, and hypothermia, but was lower in other groups including hyperthermia, in particular for asphyxia and poisoning. The CSF level was usually much higher than the serum level, but was significantly lower for hypothermia and hyperthermia than in other groups (p

The present report describes the unexpected death of a 6-month-old female infant who had been clinically diagnosed with Joubert syndrome. This is a relatively rare congenital neurological disorder characterized by hypoplasia/aplasia of cerebellar vermis, which transmits information from the body to the cerebellum, and is associated with respiratory dysfunction, abnormal eye movements, and developmental delay. The infant was found dead in bed and the immediate cause of death was determined as aspiration of vomit which may have been induced by a neurological disorder related to hypoplasia of the cerebellar vermis. These findings, together with a review of previous clinical case reports, suggest that Joubert syndrome should be considered as a predisposition to sudden unexpected death in infants mainly due to aspiration or complicated infection.

Glucose transporter 1 (GLUT1) and vascular endothelial growth factor (VEGF) have been established as being responsible for cellular adaptation to oxygen deficiency in tissue ischemia and hypoxia mediated by hypoxia-inducible factor 1. We hypothesized that mRNA quantification of these factors in autopsy tissue specimens could have diagnostic significance for investigating the pathology of death, especially after injury. Various cases (total, n = 119; less than 48 h postmortem) were examined, including fatal blunt injury (n = 71) and sharp instrument injury (n = 18), as well as asphyxia (strangulation/hanging, n = 12) and acute myocardial infarction/ischemia (n = 18) as controls. Quantification of mRNA by TaqMan real-time RT-PCR and immunostaining were performed for GLUT1 and VEGF in lung, kidney, and skeletal muscle specimens. The postmortem interval showed no significant influence on the relative quantification of mRNA during the early postmortem period. Characteristic results were found in blunt injury cases: both GLUT1 and VEGF mRNAs decreased in the lung but increased in the skeletal muscle depending on survival time. In the kidney, subacute deaths showed higher GLUT1 mRNA levels compared with acute deaths from blunt injury, but no significant change was found for VEGF mRNA. Immunohistochemistry showed visually predominant GLUT1 immunoreactivity in the renal cortex for cases with a longer survival time, coincident with the results at the mRNA level. Tissue-specific differences in mRNA quantification of GLUT1 and VEGF shed light on tissue ischemia/hypoxia and subsequent tissue-dependent pathophysiological changes leading to death after injury.

The present study analyzed serum levels of urea nitrogen (UN), creatinine (Cr), and C-reactive protein (CRP), which are very stable during the early postmortem period, for investigation of the cause of death with special regard to hyperthermia (heat stroke) in serial medico-legal autopsy cases (n = 429), excluding fatal injury, intoxication, and fire fatality. In this series, mechanical asphyxiation, drowning, and sudden cardiac death cases (n = 56, n = 43, and n = 212, respectively) usually showed low levels within postmortem reference ranges for these serum markers, although UN and CRP levels were mildly elevated in cases of sudden cardiac death and cerebrovascular stroke. There were concomitant significant elevations in serum levels of UN (>50 mg/dL), Cr (>2 mg/dL), and CRP (>2 mg/dL) for chronic renal failure, gastrointestinal bleeding, pneumonia, and hypothermia (cold exposure). UN and CRP were especially high for chronic renal failure and pneumonia, respectively. However, hyperthermia cases showed an isolated elevation in the serum Cr level, suggesting an influence of systemic skeletal muscle damage. These serum markers may be practically useful for postmortem investigation of death due to hyperthermia (heat stroke), for which specific pathological and toxicological evidence may not be available.

We report an unusual case of delayed death due to sepsis following closed blunt injury to the neck. The victim was a 71-year-old male with a clinical history of hypertension, diabetes and gout. He was found dead about three weeks after being assaulted. He had not consulted a hospital after the assault. Forensic autopsy demonstrated a large liquefied subcutaneous hematoma on the right side of the neck, peri- and thrombophlebitis of the right internal jugular vein. Otherwise, there was no evidence of trauma. Histological examination showed dermal vesicles in the skin covering the hematoma, accompanied by marked inflammatory cell infiltration phagocytosing gram-positive streptococci, subcutaneous edema, panphlebitis with partially organized thrombi and bacterial colonies, pulmonary edema and multiple pulmonary microthrombi involving bacterial aggregates. Postmortem serum C-reactive protein and neopterin levels were markedly elevated. These findings suggest sepsis as the cause of death, induced by infected internal jugular vein thrombophlebitis following blunt neck injury involving impaired skin barrier.

Catecholamines are major humoral factors and neurotransmitters that contribute to various stress responses. However, they have been considered unstable due to agony, terminal medical care and postmortem interference. The present study was a comprehensive investigation of postmortem serum levels of adrenaline (Adr), noradrenaline (Nad) and dopamine (DA) with regard to the cause of death in serial medicolegal autopsy cases (n = 542) including fatalities from various traumas and diseases. There was a slight tendency toward postmortem increases of Nad and DA in cardiac blood as well as Adr and Nad in peripheral blood, a slight age-dependent decrease in Adr and DA in right heart blood, and a marked increase in serum DA due to administration during critical medical care. When these factors were taken into consideration, significantly higher cardiac blood levels were observed for Adr and Nad in injury and asphyxiation cases and for Adr in fatal methamphetamine (MA) abuse and other poisoning cases, whereas those levels were lower in fatal hypothermia. Drowning, fire fatality, acute cardiac death and cerebrovascular disease showed intermediate Adr and Nad levels. The DA level was elevated in cases of injury, hyperthermia, MA fatality and other poisoning. Topographical analyses suggested that the major sources of increased serum catecholamines in cases of injury was abdominal viscera including adrenal glands, and that in cases of asphyxiation, drowning, fire fatality, hyperthermia, MA fatality, other poisoning, acute cardiac death and cerebrovascular disease was the extremities in addition to abdominal viscera. However, there was in part a large case-to-case difference in each marker related to individual causes of death. These findings differed markedly from clinical observations and suggest that the postmortem serum catecholamine levels may reflect the magnitude of physical stress responses during the process of death in individual cases.

We examined the immunohistochemical distributions of ubiquitin (Ub) and myoglobin (Mb) in human kidney tissues to assist the pathological assessment of death due to trauma. Medicolegal autopsy cases at our institute (n=138: 0-96 years of age, 105 males and 33 females) were examined. Causes of death were blunt injury (n=31), sharp injury (n=15), poisoning (n=11), drowning (n=10), fire fatalities (n=25), hypothermia (n=7), asphyxiation (n=14), hyperthermia (n=3), and natural diseases (n=22) for controls. Immunostaining of Ub and Mb was performed on the formalin-fixed paraffin-embedded kidney tissue sections. Quantitative analyses by estimating the proportion of Ub- and Mb-positive cells (%positivity) of renal tubule epithelial cells showed that the positivities for Ub and Mb were higher in subjects who died due to fire, blunt injury, sharp injury and fatal hypothermia than in other groups. The Ub-positivity correlated with the severity of airway thermal injury in fire deaths, survival time in blunt injury, and serum markers for renal failure in deaths due to sharp injury. Concomitant increases in the tubular Mb- and Ub-positivities were characteristic to deaths from injury and hypothermia. These findings suggest that Ub may serve as a sensitive indicator of the fatal influence of traumas.

Although previous forensic pathological studies have suggested the possible application of cardiac troponins in the diagnosis of myocardial infarction, there appears to be insufficient data with regard to its cardiac pathology. The present study analyzed the heart blood, peripheral blood and pericardial fluid levels of cardiac troponin T (cTnT) in sudden cardiac deaths (n = 96) within 48h postmortem in relation to pathological findings of acute myocardial infarction (AMI, n = 34), recurrent myocardial infarction (RMI, n = 23), ischemic heart disease without any pathological evidence of infarction (IHD, n = 24) and other heart diseases (OHD, n = 15). Control groups (n = 75, survival time

There appears to be very poor investigation of postmortem serum calcium (Ca) and magnesium (Mg) for diagnostic evidence to determine the cause of death. The aim of the present study was a comprehensive analysis of the serum levels in relation to the causes of death in routine casework. Autopsy cases (total, n = 360; 5–48 h postmortem), including blunt injury (n = 76), sharp injury (n = 29), asphyxiation (n = 42), drownings (n = 28: freshwater, n = 11; saltwater, n = 17), fire fatalities (n = 79), methamphetamine (MA) poisoning (n = 8), delayed death from traumas (n = 37), and acute myocardial infarction/ischemia (AMI, n = 61), were examined. In total cases, there was no significant postmortem time-dependent rise in serum Ca and Mg. Both Ca and Mg levels in the heart and peripheral blood were significantly higher in saltwater drowning compared with those of the other groups. In addition, a significant elevation in the Ca level was observed in freshwater drowning and fire fatalities, and in the Mg level in fatal MA intoxication and asphyxiation. Topographic analyses suggested a rise in serum Ca and Mg due to aspirated saltwater in drowning, that in serum Ca in freshwater drowning and fire fatalities of peripheral skeletal muscle origin and that in serum Mg in MA fatality and asphyxiation of myocardial and/or peripheral origin. These markers may be useful especially for diagnosis and differentiation of salt- and freshwater drownings and may be also helpful to determine the causes of death involving skeletal muscle damage, including burns and MA intoxication. # 2004 Elsevier Ireland Ltd. All rights reserved.

The aim of the present study was to examine the factors that contribute to the postmortem lung weight in acute fire fatalities (n=149) including those with lower (60%) and higher (60%) blood carboxyhemoglobin (COHb) levels (n=94 and 55, respectively). The control groups consisted of acute myocardial infarction/ischemia (AMI, n=99) and mechanical asphyxiation (n=85). For all cases (n=333), the lung and heart weights were independent of the postmortem time (4.5-72 h) and charring of the body. The combined weight of both lobes of the lung showed a significant gender difference (malesfemales, P0.001), negative regression with respect to age (R=0.167, P0.01) and positive regression with respect to heart weight (R=0.316, P0.001). The gender difference was also significant for each cause of death even after being corrected using body height measurements. When the lung-heart weight ratio was estimated to diminish the influence of possible cardiogenic factors, the gender difference was insignificant for each cause of death among the non-elderly (60 years of age). However, for elderly fire fatalities (60 years of age), there was a gender difference (malesfemales) for the lower COHb group (P0.05) and higher COHb group (P0.001). A significant age-dependent difference (non-elderlyelderly) in the lung-heart weight ratio was observed for fire fatalities with a lower COHb and AMI among males and for fire fatalities with a higher COHb among females. Such gender- and/or age-dependent influences were not significant for fatal mechanical asphyxiation. These findings suggest that a person's heart weight may be a possible contributory factor to an increase in the lung weight in acute death, and that gender- and/or age-dependent susceptibilities may be additional factors that contribute to fire fatalities and AMI. In addition, elderly females appear to be most susceptible among fire casualties, and extreme cardiomegaly may also be a potential fatal risk factor.

In the central nervous system (CNS), a variety of ubiquitinated structures have been reported, usually as pathological alterations of the brain related to degenerative diseases or aging. However, previous studies showed an increase in the ubiquitin (Ub)-immunoreactive intranuclear inclusion of the pigmented neurons of the substantia nigra in the midbrain in asphyxiation and fire fatalities in the adult subjects. The aim of the present study was to examine granular ‘dot-like' Ub-immunoreactivity in the crus cerebri (cortico-spinal tracts) in related fatalities (over 35 years of age, n =169), including fatal asphyxiation ( n =27), drownings ( n =14), fire fatalities ( n =60), and control groups ( n =68). Dot-like Ub-immunoreactivity was clearly observed in the descending tract of the crus cerebri. Morphometric analysis of the positive granular area (dot-like Ub-area) showed a higher value in strangulation and fire fatalities and a lower value in hemorrhagic and head injury deaths, as was observed for the inclusion-type neuronal Ub-positivity. However, there was a difference between those markers: a low value was seen for the inclusion-type neuronal Ub-positivity in hanging and drownings, and a difference in the dot-like Ub-area was detected between fire fatalities with lower and higher COHb levels. Our findings suggested the possible usefulness of these markers for examination of CNS stress responses in traumas, at least in middle-aged and elderly victims and a partial difference in stress reaction between the cortico-spinal tracts and dopaminergic neurons.

Serum uric acid (UA) and creatinine (Cr) mainly derive from skeletal muscle tissues. Although, remarkable postmortem stability of the serum levels has been reported, there appears to be very poor knowledge of the diagnostic value in investigation of death, except for uremia. The aim of the present study was to evaluate postmortem serum UA and Cr levels using 395 forensic autopsy cases, in comparison with blood urea nitrogen (BUN), for investigation of the pathophysiology of death with special regard to the causes of death involving possible skeletal muscle damage, e.g. due to hypoxia, heat or agonal convulsions. Cr and BUN showed relatively good topographic stability in the cadaveric blood, whereas, UA was often much higher in the right heart blood than in the left heart and peripheral blood, independent of postmortem intervals. Moderate to marked elevation of Cr and BUN accompanied with hyperuricemia was observed in delayed death. In the acute death cases (survival time30 min), UA, especially in the right heart blood, showed a considerable elevation in mechanical asphyxiation and drowning. The Cr level in fire victims with a lower carboxyhemoglobin (COHb) level (60%) was significantly higher than in those with the possible fatal level (60%). A similar elevation of Cr was observed in fatalities from heat stroke and methamphetamine (MA) poisoning. The observations suggested that hyperuricemia in acute death may be indicative of advanced hypoxia and that elevated Cr level may reflect the skeletal muscle damage, especially due to thermal influence.

Previous studies have suggested the usefulness of the postmortem serum S100B level as a marker of the severity of brain damage. In this study, we investigated the S100B level in the cerebrospinal fluid (CSF) in serial autopsy cases (n=216, within 3 days postmortem), including those of blunt injury (n=34: fatal head injury, n=20; others, n=14), sharp instrument injury (n=9), mechanical asphyxiation (n=19), drowning (n=11), fire fatality (n=26), intoxication (n=20), hypothermia (cold exposure, n=16), hyperthermia (heat stroke, n=9), acute cardiac death (n=52) and pneumonia (n=20). The CSF S100B level showed a moderate postmortem time-dependent increase for acute cardiac death (r=0.58, p0.0001) and asphyxia (r=0.741, p0.001). In cases of survival time within 48 h, drowning and hypothermia usually showed a lower CSF S100B level (around 500 ng/ml), and the level was higher for delayed head injury death, asphyxia, intoxication, and hyperthermia (around 1500 ng/ml) (p0.05). In fatal head injury cases, however, CSF S100B did not correlate with the survival time or postmortem interval. A CSF S100B level of2000 ng/ml in the early postmortem period might be considered a biochemical sign of fatally severe brain damage.

This study confirmed post-mortem ethanol concentrations in pericardial fluid and bone marrow aspirate in comparison with those in the blood in medicolegal autopsy cases (n = 140, within 48 h post-mortem). The specimens were examined by head-space gas chromatography/mass spectrometry. Ethanol concentrations in the pericardial fluid (y) were approximately equivalent to those in peripheral blood (x): y = 0.99x + 0.02, n = 44, r = 0.972. A high stomach ethanol concentration (> 10 mg/ml) appeared to mildly affect the pericardial levels. There was no significant interference in drowning cases. Ethanol concentrations in bone marrow aspirates (y) also showed a good correlation with those in the peripheral blood (x): y = 0.77x + 0.02, n = 20, r = 0.981. A dissociation was observed in cases of delayed death from hemorrhagic/traumatic shock and elderly victims. These findings suggest that pericardial fluid and bone marrow aspirate can be used as an alternative material when adequate blood specimens are not available.

Accurate estimation of the postmortem interval (PMI) has been one of the most important and complicated issues in the forensic practice. In order to provide novel perspectives for the future research concerning PMI, the advantages and disadvantages of related traditional methods, postmortem degradation of nucleic acid and tissue, the componential change of vitreous humor and histological biochemistry since 2002 have been introduced and compared in this review.

Previous studies have shown that diffuse cortical astrocyte damage is seen in acute deaths due to brain injury and mechanical asphyxiation. The present study quantitatively investigated the number of astrocytes that showed GFAP- and S100-protein immunopositivity in the cerebral white matter and hippocampus at the sites distant from primary injury with regard to survival time, complication, and the immediate cause of death of brain injury cases. Autopsy cases of brain injury (8-48 h postmortem) comprising acute/subacute deaths (survival time,3/6 h-3 days; n=27/42) and delayed deaths (survival time3 days) with/without complications (n=30/22) were examined. Delayed death cases with complications were subdivided into those in which the immediate cause of death had been determined as cerebral dysfunction (n=22) and those that had been determined as due to fatal complications (n=8). For controls, natural deaths from pneumonias (n=12) and sudden cardiac deaths (n=27) were used. In brain injury cases, the numbers of astrocytes in the cerebral white matter and hippocampal CA4 region were significantly lower for subacute death and delayed death without complications (p0.05-0.001). Delayed death with fatal complications showed a significant increase in the number of astrocytes (p0.05). Among delayed death cases, the numbers of astrocytes were higher in the cases with fatal complications than in those without complications and with non-fatal complications, although the latter cases showed large variations in the numbers of these astrocytes. These findings suggest that critical brain injury causes acute death without evident astrocyte pathology and that subacute death is associated with progressive brain damage accompanied by an astrocyte loss. In delayed death cases, the numbers astrocytes might be closely related to the severity of posttraumatic brain injury. GFAP and S100-immunopositivity might be useful for elucidating the cause and process of deaths due to brain injury.

The glial fibrillary acidic protein (GFAP) is known as a peculiar marker of mature astrocytes of the central nervous system (CNS). However, we found distinct immunopositivity to a monoclonal anti-GFAP reagent in the hippocampus neurons in head injury fatalities. The present study investigated the neuronal and neuroglial GFAP-immunopositivity in the hippocampus in a series of head injury cases, which included acute and subacute/delayed deaths (n=17 and n=73, respectively), and acute cardiac death (n=13), delayed death due to multiple organ failure from nonhead injury (n=6), and pneumonia (n=9) cases were examined as controls. GFAP-immunopositivity in the neurons was frequently observed in CA4, CA3 and CA2 regions in cases of subacute/delayed head injury death that showed marked brain swelling accompanied by secondary brain stem hemorrhages, showing an inverse relationship to that in astrocytes. These findings suggest possible induction of GFAP or a related protein in hippocampus neurons depending on the severity of brain swelling following head injury.

Basic fibroblast growth factor (bFGF) is a highly conserved and ubiquitously distributed mitogen, and much is known at the molecular level. However the available information about in vivo distribution in human tissues and expression changes in relation to causes of death is not sufficient. The present study investigated 35 autopsy cases, comprising five cases for each cause of death: acute myocardial infarction/ischemia (AMI), mechanical asphyxiation, blunt brain injury, drowning, hypothermia, intoxication and sharp instrument injury. The bFGF immunopositivity was detected mainly in interstitial cells and sporadically in cardiomyocytes in the heart, in macrophages in the lung, astrocytes in the brain, mainly in the sinusoidal Kupffer cells and partly in the hepatocytes in the liver, red pulp of the spleen, pancreatic islets and proximal convoluted tubules and corpuscles in the kidney. Immunopositivity was frequently detected in the lung and liver for AMI and hypothermia, and in the kidney for AMI, mechanical asphyxiation, drowning and injuries, but was not evident in the kidney for hypothermia. Positivity in these tissues varied by case in other causes of death. High positivity in the brain was seen for intoxication, but AMI, mechanical asphyxiation and drowning showed lower positivity. For the heart, spleen and pancreas, there was no evident difference among the causes of death. These findings suggested that bFGF expression in the lung, liver, kidney and brain varies depending on the cause of death, and is useful for investigating deaths.

Previous studies have suggested the usefulness of postmortem serum calcium (Ca) and magnesium (Mg) for investigating cause of death. The present study investigated their levels in the pericardial fluid of serial autopsy cases of adults within 48 h postmortem (n=385), including fatalities from blunt injury (n=57), sharp instrument injury (n=9), mechanical asphyxiation (n=28), salt- and freshwater drowning (n=14 and n=61, respectively), fire fatality (n=35), intoxication (n=23), hypothermia (cold exposure, n=12), hyperthermia (heat stroke, n=7), acute cardiac death (ACD, n=86), pneumonia (n=9) and spontaneous cerebral hemorrhage (n=11). The pericardial Ca level was independent of the postmortem interval, showing a value similar to that of the clinical reference range in cases other than saltwater drowning, while the Mg level was higher than the clinical reference range and showed a mild postmortem time-dependent increase. Pericardial Ca was significantly higher for saltwater drowning than other groups, and a lower level was seen for hyperthermia, and some cases of blunt injury and intoxication. The Mg level was also significantly higher for saltwater drowning than the other groups, and showed a higher level for sharp instrument injury, but a lower level for hypothermia. The Mg/Ca ratio was higher for sharp instrument injury and saltwater drowning, but was lower for hypothermia. These findings suggest that postmortem pericardial Ca and Mg can be used to investigate the cause of death, especially for saltwater drowning, hypothermia and hyperthermia.

Intracranial chordoma is a locally invasive, relatively rare tumour at the base of the skull. The tumour usually grows slowly but there have been several case reports of sudden death, all of which were due to tumour-associated haemorrhages. We report an autopsy case of a sudden unexpected death due to clinically undiagnosed intracranial chordoma in the brainstem without haemorrhage. A 44-year-old man was found dead at home. The autopsy revealed two small gelatinous and semi-translucent greyish tumours on the ventral surface of the brainstem between the midbrain and pons. The tumours were not attached to the dura or bone. The brain was markedly swollen, with enlarged lateral and third ventricles, but the aqueduct was compressed and narrowed. Microscopically, the tumour invaded the cerebral peduncles, and was classified as a chordoma. The cause of death was diagnosed as acute obstructive hydrocephalus due to a ventral brainstem tumour. Even a minor intracranial tumour that is not primarily life-threatening may cause sudden death due to subsequent obstructive hydrocephalus. The brainstem is one of the most vulnerable regions in the brain, and careful examination of this region is important for forensic pathologists.

To evaluate apoptotic neuronal damage by carbon monoxide (CO) in medico-legal autopsy cases, we investigated the immunohistochemical distribution of single-stranded DNA (ssDNA) as a marker of apoptosis and programmed cell death in the brain. Formalin-fixed paraffin-embedded brain tissue specimens, including cerebral cortex of frontal lobe, substantia nigra of the midbrain and pallidum, from medico-legal autopsy cases of fire fatality (n=63), including cases with blood carboxyhemoglobin (COHb) of a lower (60%) and a higher (60%) level (n = 39 and 24, respectively), and CO intoxication without burns (n = 6) were examined, in comparison with acute ischemic heart disease (IHD, n = 29) and asphyxiation due to strangulation (AS, n= 14). In the pallidum, neuronal immunopositivity for ssDNA was significantly higher in fire fatality with a higher COHb level than in IHD (p0.0001), and CO intoxication cases showed significantly higher positivity than other groups excluding fire fatality with a higher COHb level (p0.05). In cases without cardiopulmonary resuscitation, ssDNA-positivity in the pallidum mildly correlated to COHb concentrations (r = 0.31, p0.05), and the positivity was significantly higher in higher COHb (60%) cases than in lower COHb (30%) cases. In the cerebral cortex and substantia nigra of the midbrain, neuronal ssDNA-positivity showed no significant findings with regard to the cause of death and COHb concentration. These findings suggest that CO causes selective neuronal damage in the pallidum.

To investigate the influence of inhaling carbon monoxide (CO)-containing gases in fires, forensic autopsy cases of fire victims (n=193) were examined in comparison with control cases involving other causes of fatal CO intoxication (n=6 :COHb, 69.5-83.0%). Fire victims with blood carboxyhemoglobin (COHb) levels over 60% (n=76) showed a larger arterio-venous difference in blood COHb level compared with other fire victims and other fatal CO intoxication. However, biochemical findings for myocardial, cerebral damage or respiratory distress were milder in most cases, independent of blood cyanide levels, being similar to those in fatality due to inhalation of blast furnace gas with an extremely high concentration of CO (ca. 40%). These observations suggest that an acutely fatal factor in fires involves inhalation of gases containing high amounts of CO, which may induce peracute circulatory collapse before causing marked myocardial and cerebral damage or respiratory distress.

The present study investigated the immunohistochemical distributions and mRNA expressions of myocardial hypoxia-inducible factor (HIF)-1 alpha and its downstream factors, erythropoietin (Epo) and vascular endothelial growth factor (VEGF), in cardiac deaths. Medico-legal autopsy cases (n=114, within 48-h postmortem) of cardiac deaths (n=58) and control cases (n=56) were examined. Immunohistochemical positivities of HIF-1 alpha, Epo and VEGF were patchily observed in cardiomyocytes in the acute ischemic lesions of myocardial infarction (n=37), showing a relationship to morphological cardiomyocyte damage: the staining was intense in the regions with early ischemic changes and weak in the necrotic regions. Immunopositivities were sporadically detected in cardiomyocytes in some cases of sudden cardiac death without infarction (SCD, n=13). In chronic congestive heart disease (CHD, n=8), weak positivities were diffusely observed in the cardiomyocytes. However, there were no such findings in cases of mechanical asphyxiation (n=16) or drowning (n=18). HIF-1 alpha, Epo and VEGF mRNA expressions, as measured by real-time reverse transcription-polymerase chain reaction (RT-PCR), showed localized elevations related to acute myocardial infarction (AMI) lesions, whereas such findings were mild in recurrent myocardial infarction (RMI) and SCD cases. CHD showed significant elevations of these mRNAs irrespective of the sampling site. The mRNA expressions were significantly lower in cases of drowning. These findings suggest that focal immunopositivities and increased mRNAs of these factors are indicative of short and substantial duration of myocardial ischemia, respectively. The combined analyses may not only be useful for investigating the site, phase and severity of acute myocardial ischemia and the severity of chronic ischemic stress, but also contribute to differentiating cardiac deaths from asphyxiation and drowning or interpreting the possible contribution of cardiac disease in traumatic death.

The present study investigated cardiac troponin I (cTnI) and creatine kinase MB (CK-MB) in the blood and pericardial fluid from medicolegal autopsy cases (n=234, within 48h postmortem) with regard to the cause of death. The cTnI and CK-MB levels in cardiac, peripheral blood and pericardial fluid generally showed a mild and gradual postmortem time-dependent elevation (r=0.231-0.449, P0.05-0.001). However, postmortem elevation of cTnI was larger for specific causes of death including acute myocardial infarction (AMI), cerebrovascular diseases (CVD), hyperthermia, fatal methamphetamine (MA) abuse and carbon monoxide (CO) intoxication and insignificant for recurrent myocardial infarction (RMI), chronic congestive heart diseases (CHD) and drowning, while that of CK-MB was greater for CO intoxication and insignificant for drowning. Cardiac blood and pericardial cTnI levels were relatively high for AMI, RMI, hyperthermia, MA abuse and CO intoxication, and was low for drowning. Elevated CK-MB level was observed for cardiac blood in asphyxiation and MA abuse cases and for peripheral blood in hyperthermia and MA abuse cases. When the cTnI/CK-MB ratio was estimated, it was independent of postmortem time, and the ratios for cardiac blood and pericardial fluid were significantly higher in cases of AMI, RMI, hyperthermia and CO intoxication but lower in cases of drowning. Elevations of cTnI levels in cardiac blood and pericardial fluid were related to the morphological severity of myocardial damage. These findings suggest that elevated cTnI and CK-MB levels in blood and pericardial fluid are related to ischemic, hypoxic and/or cytotoxic myocardial damage, which are characteristic of the cause of death, although the levels increase after death depending on myocardial damage at the time of death.

Previous studies showed significant differences in postmortem urea nitrogen (UN), creatinine (Cr) and uric acid (UA) levels in heart blood depending on the causes of death, including acute death. In addition, the levels in pericardial fluid approximated the clinical serum reference ranges, and their elevations may be assessed based on clinical criteria. The present study investigated difference between blood and pericardial levels of these markers. Medicolegal autopsy cases (n=556, within 48h postmortem) of the following causes of death were examined: injury (n=136), asphyxiation (n=50), drowning (n=39), fire fatalities (n=99), hyperthermia (n=11), hypothermia (n=8), poisoning (n=26), delayed traumatic death (n=44) and natural diseases (n=143). When serum UN, Cr and UA levels were compared with the pericardial levels, there was an equivalency for delayed traumatic death and chronic renal failure, although each level was markedly elevated. Parallel increases in serum and pericardial UA and/or Cr levels were also observed for hypothermia and gastrointestinal bleeding. However, in drowning cases, the left cardiac and pericardial UN levels were lower than the right cardiac and peripheral levels, suggesting the influence of water aspiration. Significant elevations in serum and pericardial Cr and UA levels with a higher serum/pericardial UA ratio for fatal methamphetamine intoxication suggest progressive skeletal muscle damage due to advanced hypoxia/acidosis. Similar findings were often observed for other acute and subacute deaths. These findings suggest that a comparison between blood and pericardial nitrogenous compounds would be useful for investigating the cause and process of death.

This report describes a rare autopsy case of death due to gallbladder injury. The victim was a 63-year-old man, with a clinical history of liver cirrhosis and alcohol abuse. The postmortem examination revealed fatal hemoperitoneum from traumatic gallbladder avulsion. Related injuries were observed in the right hypochondriac region. Normal distended gallbladder, liver cirrhosis and alcohol abuse were considered to be the predisposing factors. The gradual development of bleeding from the small vessels of the gallbladder and the liver bed may have caused extensive hemoperitoneum.

Accumulating studies demonstrate that the expressions of hypoxia-inducible factor 1 (HIF-1), erythropoietin (EPO) and vascular endothelial growth factor (VEGF) depend on cellular oxygen tension, which is involved in the pathological process of tissue hypoxia and/or ischemia. The present study investigated hypoxia-inducible factor-1alpha (HIF-1alpha), EPO and VEGF mRNA expressions in the kidney with regard to the cause of death in medicolegal autopsy. Relative quantifications of HIF-1alpha, EPO and VEGF mRNAs, based on real-time TaqMan reverse transcription-polymerase chain reaction (RT-PCR), were performed on tissue specimens obtained from consistent sites of the bilateral renal cortices. The cases (total, n=245, 6-48h postmortem) included fatal blunt/sharp instrument injuries (n=53/31), asphyxia (n=28: aspiration, n=8; strangulation/hanging, n=20), drowning (n=27), fire fatality (n=62), acute myocardial infarction/ischemia (AMI, n=39), and gastrointestinal hemorrhage (n=5). Both HIF-1alpha and EPO mRNA levels were significantly lower in drowning cases. More characteristic findings were found for VEGF mRNA: it showed higher expression levels for AMI, acute blunt/sharp instrument injury, and aspiration, whereas it was lower for neck compression (strangulation/hanging), drowning, fire fatality with higher blood carboxyhemoglobin (COHb) levels (>60%), peracute blunt injury, and gastrointestinal hemorrhage. Quantitative assays of renal HIF-1alpha, EPO and VEGF mRNA transcripts are potentially useful for investigating the pathophysiology of death, and VEGF mRNA may be especially useful as an indication of acute circulatory failure.

Recent advances in molecular biology have suggested the potential usefulness of mRNA analyses in postmortem investigations of fatal mechanisms. The aim of the present study was to establish quantitative assays of oxygen-regulated factors including erythropoietin (EPO), vascular endothelial growth factor (VEGF) and hypoxia-inducible factor 1 alpha (HIF1A) mRNAs, and to investigate the postmortem stability of these mRNA transcripts in forensic autopsy materials. Relative quantification of EPO, VEGF and HIF1A mRNAs, based on the TaqMan reverse transcription-polymerase chain reaction (RT-PCR), was performed on autopsy tissue specimens from the heart (n = 10), brain (n = 10), kidney (n = 16) and lung (n = 8) after preservation at room temperature for various storage times. VEGF and HIF1A mRNA gradually degraded in patterns similar to glyceraldehydes-3-phosphate dehydrogenase (GAPDH) mRNA used as an endogenous reference. Accordingly, the relative quantification of VEGF/GAPDH and HIF1A/GAPDH changed little up to 48h postmortem in tissue samples from the brain, kidney and lung except for a mild deviation of HIF1A in the myocardium. However, the status was different for EPO mRNA, with extraordinary stability for postmortem degradation and a marked postmortem time-dependent increase in the EPO/GAPDH ratio for all tissue samples. The present study suggested the potential for applying quantitative analyses of mRNA transcripts to autopsy materials and indicated the significance of investigating degradation profiles prior to carrying out relative quantification of target mRNAs in autopsy materials.

Clusterin is a glycoprotein known to play various physiological roles including complement activity, amyloid binding activity in Alzheimer disease, as well as binding with heat shock proteins and abnormal prions. The present study immunohistochemically investigated the expression of clusterin in the human pituitary gland in subjects of 10-88 years of age (n=173). Causes of death were blunt injury (n=35), sharp injury (n=15), poisoning (n=11), drowning (n=14), fire fatalities (n=28), asphyxiation (n=15), hypothermia (n=7), hyperthermia (n=3), and natural diseases (n=45). Clusterin was detected in mixed cell follicles and the anterior lobar parenchymal cells. The area occupied by cells positive for clusterin were measured, and the ratio to the whole area of the anterior lobe (% clusterin-positive cell area) was estimated. There was a good correlation between the age of the subjects in years and the % clusterin-positive cell area in the anterior lobe of the pituitary gland (r=0.736, P0.01). Relationships between % clusterin-positive cell and gender, cause of death, and survival time were insignificant. These findings indicate an age-dependent accumulation of clusterin in the pituitary gland, which may be related to the aging of endocrine systems.

The hypophysis is embedded in the fossa at the base of skull, having important functions in the hormonal system. The present study investigated its postmortem morphological changes and the stability of adenohypopyseal hormones. The pituitaries were collected at autopsy 6 h to 20 days postmortem and were studied by histology, immunohistochemistry and electron microscopy. To avoid the influence of prolonged brain hypoxia or swelling, subjects who survived not longer than 12 h were examined. Histological changes were seen in the nucleus 6 h after death, followed by cytoplasmic changes, and the cell shapes were hardly identifiable 7 days postmortem. Electron microscopy revealed evident ultra-structural changes 6 h postmortem, involving rough endoplasmic reticulum, Golgi complexes, mitochondria, nuclei and cell membranes. However, secretory granules remained well preserved 7 days postmortem. Immunostaining showed positivities for growth hormone, prolactin, adenocorticotropic hormone, luteinizing hormone and thyroid-stimulating hormone up to 15 days after death. These findings suggest the usefulness of immunohistochemical investigation of the adenohypophysis for estimating the time of death and endocrinologic evaluation in decomposed cadavers.

In forensic pathology, previous studies have suggested the possible application of cardiac troponins in the diagnosis of myocardial infarction. However, there appears to be insufficient practical data on other causes of death. The present study was a comprehensive analysis of the cardiac, peripheral blood and pericardial levels of cardiac troponin T (cTnT) in serial medicolegal autopsy cases (n = 405) with a survival time

S-100 protein (S100) is an acidic calcium-binding protein, which is abundantly found in the brain. The aim of the present study was to investigate the immunohistochemical distribution of S100 in the cerebral cortex in forensic autopsy cases with regard to the cause of death and relationship to its serum levels. The cases (n = 286, 3-48 h postmortem) included fatal head injuries (n = 89), acute death from other blunt injuries (n = 29), sharp instrument injuries (n = 20), asphyxiation (n = 29: strangulation/hanging, n = 22; aspiration, n = 7), drownings (n = 22), fire fatalities (n = 68), cerebrovascular diseases (n = 9) and acute myocardial infarction/ischemia (AMI, n = 20). S100-immunopositivity was mainly observed in the gliacytes, in part, in the neurons and myelins. For S100B-immunostaining, the gliacytes and myelins were positive, whereas the neurons were negative. Positivity in astrocytes was dependent on the cause of death, and was significantly lower in acute deaths due to strangulation/hanging and drowning, and mildly low in those due to injuries. Positivity in neurons and myelins was frequently observed in delayed head injury deaths and fire fatalities, showing an inverse relationship with the positivity in astrocytes in head injury cases. For cases of acute death, there was an inverse relationship between S100-positivity in the astrocytes and the serum S100B level. These observations suggest that astrocytes are more rapidly and severely injured than neurons during fatal brain damage, thereby causing an elevation in the serum S100B level.

Five autopsy cases were examined to investigate fatal factors involved in inhalation of "asphyxiant gases": carbon monoxide (CO, n=3), fluorocarbons (n=1) and butane (n=1). In all cases, there was severe pulmonary edema and congestion in all viscera, suggesting advanced circulatory failure. The airway was filled with bloody froth in cases of fluorocarbons and butane inhalation. In CO intoxication, a marked increase in serum cardiac troponins suggested severe myocardial damage. There were also biochemical findings of respiratory distress (an evident increase in intra-alveolar pulmonary surfactant protein A), alveolar injury (an increase in serum surfactant protein A and D), rhabdomyolysis (myoglobinuria) and prolonged hypoxia (myogenic hyperuricemia) in cases of inhaling incomplete combustion gases. In a case of fluorocarbons gas inhalation, biochemical findings suggested respiratory distress, myocardial ischemia (an increase in serum CK-MB) and advanced hypoxia. Similar findings were observed in a case of butane inhalation, although cardiac troponin levels were low in the peripheral blood. These observations suggested that myocardial damage was prominent in CO intoxication, accompanied by respiratory distress in cases of inhaling incomplete combustion gases, whereas respiratory distress and hypoxia were major findings in cases of fluorocarbons and butane gas inhalation.