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von Willebrand factor (VWF) plays a crucial role in hemostasis and thrombosis. VWF is involved in platelet attachment to the subendothelium, serving as a carrier protein for coagulation factor VIII. In this study, myocardial tissues from deceased patients with ischemic heart disease and a mouse model of acute myocardial infarction were subjected to immunohistochemistry to determine VWF expression. We examined 28 neutral formalin-fixed, paraffin-embedded myocardial tissue samples obtained from the autopsies of patients who were diagnosed with ischemic heart disease within 48 h postmortem. Most myocardial cells were negative for VWF, although some cells showed nonspecific positivity. Elevated VWF expression was observed around myocardial cells undergoing remodeling, suggesting that endothelial proliferation occurred at these sites. In contrast, completely fibrotic myocardial foci did not show upregulated VWF expression. Positivity in fibrin deposition and hemorrhagic sites was observed. The same VWF expression characteristics as those observed in the human samples were observed in the mouse model. VWF immunostaining as an endothelial marker may be a useful supplementation to conventional staining techniques that are currently used in the diagnosis of ischemic heart disease in terms of examining the timing of myocardial remodeling in detail and highlighting the remodeling process.

Background Syphilis is caused by the bacterium Treponema pallidum. Syphilis is a multistage disease, and the clinical stages of syphilis are divided to primary, secondary, and tertiary syphilis, where the tertiary stage is classified as neurosyphilis, cardiovascular syphilis, or gummatous syphilis. Here, we describe an autopsy case of acute pulmonary thromboembolism with neurosyphilis. Case presentation A male in his early 40s began to complain of hallucinations. He was admitted to a psychiatric hospital as an emergency case 4 days before death. He was physically restrained to control agitation and aggressiveness. The patient was severely obese (BMI 36.45). At autopsy, large thromboembolic masses filled the pulmonary trunk and both pulmonary arteries. Thrombi were also noted in the right popliteal vein and bilateral gastrocnemius and soleus veins, suggesting bilateral lower extremity deep vein thrombosis. Dissection of the brain, which weighed 1457 g, revealed no noteworthy macroscopic findings. Histological examination showed lymphocyte infiltration into the perivascular space of the brain tissue with no vasculitis. Immunohistochemical staining of T. pallidum was negative, the fluorescent treponemal antibody-absorption test was positive, the rapid plasma reagin titer was 1:4, and the T. pallidum hemagglutination assay titer was 1:10,240. Real-time PCR assay of the brain tissue detected low copy numbers of T. pallidum genes. Altogether, the cause of death was acute pulmonary thromboembolism resulting from bilateral lower extremity deep vein thrombosis. The patient also had early-stage meningovascular neurosyphilis. Conclusion An autopsy case of acute pulmonary thromboembolism with meningovascular neurosyphilis is presented, including histopathological examination, serological assessment, and genetic testing. Forensic pathologists should pay attention to a myriad of syphilitic manifestations. The contributing factors for thrombosis in the present case included severe obesity, probable dehydration, and physical restraints implemented to control meningovascular neurosyphilis-induced neuropsychiatric symptoms.

A crossbow is a bow that shoots an arrow when a gun-like trigger is pulled. Deaths caused by accidental crossbow shootings are extremely rare. Here we describe an autopsy case of a penetrating wound to the left cerebral hemisphere caused by an accidental shooting with a crossbow. A man in his early 60s who lived with his wife and had used crossbows for 20 years as his hobby was found one early morning in the shed of his house, collapsed and bleeding from the head and neck. He was taken to a hospital and died after approximately 3 days of conservative treatment. At autopsy, a penetrating wound between the upper part of the left anterior neck and the left frontoparietal region was evident. Traumatic intracerebral hematoma was observed in the left frontal lobe, and severe traumatic subarachnoid hemorrhage was present throughout the brain. Cerebral contusion and hematoma without any organization were noted around the penetration. The cause of death was determined to be cerebral contusion and intracerebral hematoma due to the penetrating wound by the crossbow arrow. He was probably trying to load an arrow into the crossbow by placing it on the floor, pointing upward, and made a mistake in its operation that resulted in the shooting of the arrow. This case is unique because it was a rare accidental death caused by a crossbow arrow, and a detailed histopathological examination was performed.

Thrombomodulin is a transmembrane glycoprotein that is ubiquitously expressed on the surface of vascular endothelial cells. Thrombomodulin exerts its anticoagulant effects by combining with thrombin, activating protein C, and inactivating the coagulation factors FVa and FVIIIa. Clinically, thrombomodulin is also known as a marker of vascular injury because it circulates freely in response to endothelial injury. In this study, myocardial tissue from cases of ischemic heart disease was subjected to immunohistochemistry by thrombomodulin. We examined 40 neutral-formalin-fixed, paraffin-embedded myocardial tissue samples from autopsy cases that were diagnosed with ischemic heart disease (within 48 h postmortem). Thrombomodulin expression was observed in vascular endothelial cells between myocardial cells and in mesothelial cells of the epicardium. In necrotic myocardium, diffusion of thrombomodulin, which reflected endothelial injury, was observed. Upregulated thrombomodulin expression was observed around myocardial cells under ongoing remodeling, which suggested endothelial proliferation in these locations. Completed fibrotic foci of the myocardium did not show upregulated thrombomodulin expression. In a mouse model of acute myocardial infarction, the same phenomena as that found in human samples were observed by immunohistochemistry of thrombomodulin. Immunostaining of thrombomodulin, as a marker for endothelial injury or myocardial remodeling, may be useful for supplementing conventional staining techniques in the diagnosis of ischemic heart disease in forensic pathology.

The deceased was a 44-year-old male who was treated for a suspected Ebstein's anomaly observed using transthoracic echocardiogram. He was found dead in his bed at home. Autopsy revealed that the septal tricuspid leaflet was intact; however, a large anterior tricuspid leaflet cleft and right atrioventricular cavity dilation were observed. Pathological examination revealed a normal tricuspid valve, except for the presence of a cleft with local fibrosis of the left ventricle papillary muscle and hemosiderin-containing macrophages at both lungs. There were no other abnormalities that may have led to death. It was concluded that he died a cardiac death based on the right heart overload associated with the anterior tricuspid leaflet cleft. This case indicates the possibility that the anterior tricuspid leaflet cleft can cause death and also highlights the necessity of a detailed autopsy to accurately diagnose the cause of death.

Rosai–Dorfman disease (RDD) is a rare non-Langerhans cell histiocytosis that is characterized histopathologically by accumulation of CD68-positive, S100-positive, and CD1a-negative histiocytes. Cardiac involvement of RDD is rare. We report here an autopsy case of cardiac involvement of RDD presenting as fibrinous pericarditis. A 14-year-old Japanese boy complained of loss of appetite and breathing difficulty when lying down. He was found dead on his back in his bedroom. One year before his death, he was diagnosed with RDD after skin biopsy. At autopsy, the deceased was 153 cm in height and weighed 38 kg with systemic edema. He had flat pigmented light-brown spots, as well as many pale reddish-brown papules on the abdomen and both thighs. Cervical and mediastinal lymphadenopathy was observed. A large amount of pleural and ascitic fluid was observed. The spleen weighed 381.9 g and showed splenomegaly. The heart weighed 620 g and showed acute fibrinous pericarditis with adhesion. Abundant fibrin was observed on the epicardial surface. The infiltrating cells were CD68-positive, S100-positive, and CD1a-negative histiocytes. The skin and spleen showed histiocytic involvement. Systemic edema, large amounts of pleural and ascitic fluid, a high brain natriuretic peptide level in blood, and hemosiderin-laden macrophages in the lungs suggested chronic heart failure. We speculate that the cause of death was extranodal cardiac involvement of RDD with chronic heart failure. This case highlights the need for forensic pathologists to perform a complete autopsy to determine the cause of sudden death when cardiac involvement of RDD is present.

We report an autopsy case of hemopericardium caused by rupture of a ventricular aneurysm associated with acute myocarditis in an infant boy aged 2years and 10months. Three days before his death, the patient developed fever. On the day of death, he described an urge to defecate and attempted to do so in an upright position. While straining to defecate without success for a prolonged period, he stopped breathing and collapsed. On autopsy, his heart weighed 91.7g and cardiac tamponade was evident, the pericardial cavity being filled with 140mL of blood that had come from a 1.5-cm-long rupture in a 2.7×1.5cm ventricular aneurysm in the posterior left ventricular wall. Patchy grayish-white discoloration was noted in the myocardium. Histologically, CD3-positive T lymphocytic infiltration accompanied by pronounced macrophage infiltration was observed in the myocardium. Hemorrhagic necrosis was detected in the area of the ventricular aneurysm. Staining for matrix metalloproteinase (MMP) expression revealed abundant MMP-2, MMP-7, and MMP-9. Polymerase chain reaction to detect viruses failed to identify any specific causative viruses in the myocardium. In this case of lymphocytic (viral) and histiocytic myocarditis with pronounced macrophage infiltration and upregulation of MMP expression, myocardial remodeling and associated wall weakening had resulted in formation and rupture of an aneurysm.

A Japanese woman in her 30s was found dead on a mattress. She had had fever, cough, and dyspnea for about 2 weeks. Gross examination at autopsy revealed slight enlargement of the thyroid gland and histopathological examination resulted in a diagnosis of chronic lymphocytic thyroiditis. The concentration of triiodothyronine in the cadaveric blood was extraordinarily high, whereas that of thyroid stimulating hormone was below the detection limit. Autoimmune antibodies against thyroid tissue were positive. The cause of death was assumed to be congestive heart failure caused by thyroid storm associated with chronic lymphocytic thyroiditis. Systemic histopathological examination of tissues and postmortem biochemistry can enable a diagnosis in medicolegal autopsies.

A Japanese man in his 30s who had congenital cerebral palsy was found unresponsive in bed. His death was confirmed after resuscitation attempts. He had a history of occasional falling (despite the use of walking sticks and a wheelchair) owing to a slowly progressive gait disturbance, and had a medical examination without full neurological re-examination. Autopsy revealed gangliocytoma in the medulla oblongata, which was diagnosed as the cause of death. Although gangliocytoma is a well-differentiated benign tumor, the almost total replacement of the medulla oblongata by the tumor cells was assumed to result in ataxia via the olivocerebellar tract and secondary cerebellar atrophy, followed by central hypoventilation and death of the patient. The symptoms caused by gangliocytoma may be overlooked owing to long-standing cerebral palsy.

A man in his thirties was found dead in bed. He had undergone repair of a ventricular septal defect in his infancy and had a 2-month history of antemortem chest pain. On autopsy, a ruptured saccular aneurysm of the ascending aorta was identified, and the right thoracic cavity was found to contain coagulated blood. The oval ostium of the aneurysm was smoothly endothelialized and a black suture was found near its edge. Histological analysis revealed a defect of the intimal and medial layers in the wall of the aneurysm and hypertensive changes in several organs. The cause of death was presumed to be the rupture of a pseudoaneurysm at the aortic cannulation site after a long postoperative period. In the present case, preexisting hypertension was suspected as the cause of the formation and rupture of the pseudoaneurysm. In case of unexpected death, it is important to examine the past medical history even after a long postoperative period.

A 21-day-old Japanese male infant became inactive and then collapsed unexpectedly. On autopsy, there was no connection between the ascending and descending thoracic aorta. The site of interruption was the aortic isthmus. The heart showed hypertrophy and exhibited intracardiac malformations, including subaortic valve stenosis resulting from posterior deviation of the ventricular outlet septum and ventricular septal defect. The cause of death was diagnosed as prolonged physiological closure of the ductus arteriosus complicated by interrupted aortic arch and followed by assumed ductal shock.

Coronary artery aneurysm is a fairly uncommon clinical entity, which is defined by a characteristic dilatation that exceeds 1.5 times the width of normal adjacent coronary artery segments. In the present report, we describe a case of rupture of a massive coronary artery aneurysm. A man in his 40 s was found dead in his bed. The pericardial cavity contained 270 mL of blood with 428.2 g of coagulation. Two true aneurysms of the right coronary artery were identified. A proximal aneurysm, adjacent to the right auricle, had ruptured on the right. A distal unruptured aneurysm was identified 5.1 cm distal to the proximal ruptured aneurysm. Atherosclerosis of the coronary arteries and aorta was severe. The heart weighed 799.1 g and showed concentric ventricular hypertrophy, myocardial thinning, and patchy fibrosis. Histological analysis showed that both aneurysms were purely atherosclerotic true aneurysms without considerable inflammation. The cause of death was determined as cardiac tamponade due to rupture of a giant coronary atherosclerotic aneurysm.

We proposed a pedestrian movement support system using visible-light communication (VLC) with light-emitting diodes (LEDs) for the people of weak eyesight and the elderly. It provides the user safety information in the neighborhood or the route information, and receives a request from the user and traffic information by the LED light. We conducted visibility evaluation experiments with visually impaired people to satisfy the quality of experience for flickerfree. We created three-types of hands-free receiver (neck, arm, and white cane) of the navigation system to inform danger condition and/or obstacles such as steps and signals. The prototype was evaluated by visually impaired users, clarifying the effectiveness of the system.

This chapter analyzes the role of women’s self-help networks in anti-caste discrimination movements in Nepal. Focusing on the women of the Khadgi caste, who have historically been engaged in slaughtering, processing, and trading livestock (their caste-ordained role) and suffered from discrimination as “low caste,” I will describe shifts in strategies in their networking process during anti-caste discrimination movements of the 1950s, 1990s, and 2000s.

Background and Aims: Enteroscopic observation has clearly demonstrated that non-steroidal anti-inflammatory drugs/low-dose aspirin (usually enteric-coated) induces hemorrhagic lesions, including ulcers and bleeding, in the small intestine of patients at a high incidence. Such intestinal lesions induced by NSAIDs have been confirmed in animal experiments. With aspirin, however, it has long been believed that it is difficult to induce any damage in the intestinal mucosa of laboratory animals. Therefore, we established a new method of inducing intestinal hemorrhagic lesions in rats by injecting aspirin into the proximal duodenum. Methods: Under ether anesthesia, aspirin (50–200 mg/body), suspended in 2% methylcellulose (with or without 0.1 N HCl), was injected into the proximal duodenum of normally fed or 20-h non-fed rats (male Sprague–Dawley, 9 weeks old). At 1 h after treatment, the animals were killed with ether and the entire small intestine was removed for histological examination. In some experiments, 1% Evans blue was injected (i.v.) into the rats 1 h after aspirin treatment to visualize the lesions. An image analyzer determined the total area of the intestinal lesions. Oral proton pump inhibitors and histamine H2-receptor blockers were given 1 h before aspirin injection. 16,16-dimethyl prostaglandin E2 (dmPGE2) was given s.c. 30 min before aspirin injection. Results: Aspirin alone clearly induced severe lesions (including bleeding and ulcers) mainly in the jejunum at 100% incidence. Total score of lesions per rat obtained by histological examination was similar to the damaged area quantified with the dye method. Dose-related induction of lesions by aspirin was confirmed both by the histological and dye methods. The irritable effect of aspirin suspended in 0.1 N HCl solution was the same as that of aspirin alone; 0.1 N HCl alone induced only minor lesions in the intestine. Both proton pump inhibitors and histamine H2-receptor blockers, at doses that inhibit gastric acid secretion, had no or little effect on aspirin-induced intestinal lesions. Pretreatment with dmPGE2 (3, 10, 30 µg/kg) showed significant prevention of both aspirin- and HCl/aspirin-induced intestinal lesions. Conclusion: This new aspirin lesion model will be useful for screening defensive drugs against aspirin-induced intestinal lesions and to elucidate the underlying mechanism.

Sudden death while bathing is a major issue in elderly Japanese individuals. Despite its growing incidence, the exact processes underlying sudden death while bathing remain unknown. This study was designed to establish reliable diagnostic markers for drowning while bathing, as well as to assess the pathological conditions associated with sudden death while bathing, by analyzing the immunohistochemical intensity and localization of surfactant protein-A (SP-A), heat shock protein 70 (HSP70) and c-Fos protein in the lungs and central nervous system, including the cerebral cortex and hippocampus. We found that a distinct pattern of immunohistochemical expression of SP-A, HSP70 and c-Fos in the lung can be utilized to diagnose drowning. In most of these individuals, c-Fos protein was absent from the central nervous system, providing insight into patterns of ischemia in the central nervous system, or a loss in consciousness while bathing. We also found that rapid hypothermia or a cold stimulus increased c-Fos expression in the hippocampus (CA4). Furthermore, our results suggest that HSP70 expression in the hippocampus (CA4) can be used to estimate the length of time between the initial occurrence of stress and death.

A case of sexual asphyxial death by hanging is presented. A 35-year-old male, found dead lying on his face in a bed of a truck cab, had hanged himself from a window frame using a leather belt. He was completely naked. There were pornographic and sadomasochistic magazines beneath his face, opened to pages depicted nude photographs of a woman. Autopsy findings revealed a ligature mark on the neck and petechial hemorrhages in the conjunctivae, but there were no hemorrhages in the neck muscles or fractures of the hyoid bone or the thyroid cartilage. The alcohol levels in the blood and urine were 0.78 and 0.45 mg/ml, respectively. The circumstances suggested that his death was accidental, and due to asphyxia by hanging performed to enhance sexual gratification during masturbation. Sexual asphyxia is reviewed and discussed.

An accidental atypical hanging with the collar of a sweater is reported. A 67-year-old man was found dead in the sitting position with the collar of his sweater hanging off the brake handle of a motorcycle. Autopsy findings revealed a ligature mark on the surface of the neck; hemorrhages in the sternohyoid muscles; submucosal hemorrhages in the left greater horn of the hyoid bone; a large degree of submucosal petechial hemorrhages in the larynx, oral mucosa, and palpebral conjunctivae; and dark-red liquid blood with little clotting in the heart cavities. The alcohol levels in the blood and urine were 2.84 mg/ml and 3.52 mg/ml, respectively. It was concluded that the man had died from hanging by the sweater, and it was speculated that when he became inebriated, he might have lost consciousness and then fell with the collar of his sweater hanging from the brake handle of the motorcycle.

We here report a 60-year-old woman in whom autopsy revealed a metastasis in the right cardiac ventricle from a well-differentiated squamous cell carcinoma (SCC) of the left hand. The tumors in the myocardium and left hand were both well-differentiated SCCs with keratinization and sporadic keratin pearls. High concentrations of heart failure markers together with a pericardial effusion suggested antemortem chronic heart failure. Our case is particularly unusual because there were no regional lymph node metastases and the cardiac metastasis was not one of multiple metastases; thus, hematogenous metastasis to the right side of the heart alone had occurred.