Problems of "death at home" during home care

In Japan, with the progress of aging society, home care will be promoted due to alteration of social security in near future. In these circumstances, increase of "deaths at home" is expected. Thus as "death at home" increase, it is suspected that physicians will have to investigate and diagnose in the case of "death at home" more frequently than the present time. In this review, on the basis of the laws and regulations, we describe the issue of death certificate or postmortem examination of "death at home", and the roles of "family doctors" for home care

Formation experiments of CO2 hydrate chimney in a pressure cell

Experimental investigations were conducted to understand the formation process of CO_2 hydrate the chimney structure by using a gas bubble emission technique in water within a pressure cell. The detailed process was video-recorded and analyzed to study the initiation and growth behavior of hydrate chimney while the cell pressure was increased and gas supply rate decreased gradually with time. In the initial stage of chimney growth, a hydrate crystal started to form in a cup shape at the gas nozzle and ascended together with gas bubbles due to mechanical weakness of the hydrate/nozzle contact. Growth of hydrate chimney occurred with supercooling of 3K(overpressure of 0.60MPa) or more, and continued until the top end was closed completely by hydrate

Transplantation of genetically marked cardiac muscle cells

AbstractWe examined the possibility that cardiomyocytes could be genetically marked or modified before being grafted to the heart under conditions applicable to the clinical setting. We used a replication-defective recombinant adenovirus carrying the β-galactosidase reporter gene, and delivered it to cultured murine fetal cardiac myocytes. Virtually all fetal cardiomyocytes in a primary culture expressed β-galactosidase 24 hours after recombinant adenovirus infection. These cells were transplanted to the hearts of syngenic adult recipient mice. Expression of the β-galactosidase gene in the grafted cells was demonstrated by staining with 5-bromo-4-chloro-3-indoyl-β-d-galactosidase, resulting in a blue color at the histochemical level and an electron-dense deposit on transmission electron microscopic analysis. Gene expression was recognized from 7 days to 12 weeks after transplantation. Implanted cardiomyocytes aligned themselves along the layers of the host myocardium. Formation of gap junctions was demonstrated by transmission electron microscopy. Neither inflammation nor fibrous scar tissue was detectable by histologic analysis. This study demonstrates that ex vivo gene transfer to the heart by means of the adenoviral vector is possible. (J Thorac Cardiovasc Surg 1997;113:10-8

FoxO1 Gain of Function in the Pancreas Causes Glucose Intolerance, Polycystic Pancreas, and Islet Hypervascularization

Genetic studies revealed that the ablation of insulin/IGF-1 signaling in the pancreas causes diabetes. FoxO1 is a downstream transcription factor of insulin/IGF-1 signaling. We previously reported that FoxO1 haploinsufficiency restored β cell mass and rescued diabetes in IRS2 knockout mice. However, it is still unclear whether FoxO1 dysregulation in the pancreas could be the cause of diabetes. To test this hypothesis, we generated transgenic mice overexpressing constitutively active FoxO1 specifically in the pancreas (TG). TG mice had impaired glucose tolerance and some of them indeed developed diabetes due to the reduction of β cell mass, which is associated with decreased Pdx1 and MafA in β cells. We also observed increased proliferation of pancreatic duct epithelial cells in TG mice and some mice developed a polycystic pancreas as they aged. Furthermore, TG mice exhibited islet hypervascularities due to increased VEGF-A expression in β cells. We found FoxO1 binds to the VEGF-A promoter and regulates VEGF-A transcription in β cells. We propose that dysregulation of FoxO1 activity in the pancreas could account for the development of diabetes and pancreatic cysts

One autopsy case of an elderly traffic accident victim with Tetralogy of Fallot

The case of a61-year-old male traffic accident victem with Tetralogy of Fallot (TOF) is reported. The autopsy revealed massive hemorrhages in the subcutaneous tissue, muscle, and subarachnoidal space. Furthermore, multiple fractures of ribs, sternum and thoracic vertebrae were observed. Histopathological examination revealed changes characteristic of trauma, such as acute lung congestion, acute renal cortical necrosis, and embolization in the lungs and kidney. These autopsy and histological observations indi-cated that traumatic shock was cause of his death. Moreover, histologically, we observed changes due to his congenital heart disease, such as right ventricular hypertrophy, heart failure cells in the lungs, sclerosis of the liver, and hyaline degeneration in the kidney. Furthermore, ischemic changes, shrinkage or loss of neurons, were seen in hippocampus, and swelling of astrocytes in both cortex and hippocampus were also observed. These observations lead us to speculate that a hypoxic episode may have caused his accidental death while driving

Pyrogallol inhibits NFAT signal

As the expression level of allergic disease sensitive genes are correlated with the severity of allergic symptoms, suppression of these gene expressions could be promising therapeutics. We demonstrated that protein kinase Cδ / heat shock protein 90-mediated H1R gene expression signaling and nuclear factor of activated T-cells (NFAT)-mediated IL-9 gene expression signaling are responsible for the pathogenesis of pollinosis. Treatment with Awa-tea combined with wild grape hot water extract suppressed these signaling and alleviated nasal symptoms in toluene-2,4-diisocyanate (TDI)-sensitized rats. However, the underlying mechanism of its anti-allergic activity is not elucidated yet. Here, we sought to identify an anti-allergic compound from Awa-tea and pyrogallol was identified as an active compound. Pyrogallol strongly suppressed ionomycin-induced up-regulation of IL-9 gene expression in RBL-2H3 cells. Treatment with pyrogallol in combination with epinastine alleviated nasal symptoms and suppressed up-regulation of IL-9 gene expression in TDI-sensitized rats. Pyrogallol itself did not inhibit calcineurin phosphatase activity. However, pyrogallol suppressed ionomycin-induced dephosphorylation and nuclear translocation of NFAT. These data suggest pyrogallol is an anti-allergic compound in Awa-tea and it suppressed NFAT-mediated IL-9 gene expression through the inhibition of dephosphorylation of NFAT. This might be the underlying mechanism of the therapeutic effects of combined therapy of pyrogallol with antihistamine

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

トウシ ノ イチボウケンレイ

In 30th April, 72-years-old male was found dead in the grass near a farm road in TokushimaCity. An autopsy revealed that he was very thin, and rectal temperature,22℃, was relativelow against other postmortem changes. Furthermore, the left cardiac blood was brightpink, so there was markedly different between the color of right and left cardiac blood. Thelungs were collapse. From those autopsy findings, his cause of death was diagnosed the fatalhypothermia. Besides cause of death, autopsy also revealed ascites and liver tumor.Histopathologically, adenocarcinoma was observed in liver, pancreas and kidney. His heartwas slackened. Myocardial fibers were thin and intricate, and heart failure cells were observedin lungs, histopathologically. He had been operated stomach cancer, so it seems thatthe cancer has spread to liver and other organs. Those findings suggested that he failed intocachexia with chronic heart failure and metastasis carcinoma. The cachexia strongly contributedhis cause of death, fatal hypothermia

An autopsy case of adrenal insufficiency 20 years after Hypophysectomy:Relation between stress and cause of death

A 63-years-oldman 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 in sufficiency. 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-OHCSin 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

Immunohistochemical diagnosis and significance of forensic neuropathological changes

Immunohistochemistry is very useful when investigating the cause of death. Ischemic cell changes in the hippocampal neurons were not obvious in the brains damaged by hypoxic injury. However, it is suggested that even a moderate hypoxia, which may affect the neuronal proteins and metabolism, induced astrocytes is in the CA3 and CA4 regions, and that in patients with a history of hypoxic attacks neuronal damage may be severe even several hours after ischemic injury. Furthermore, hsp70 expression was found in the CA2, CA3 and CA4 regions of long-term survivors after severe hypoxic / ischemic injury. In forensic practice, detailed information about the duration and extent of a hypoxic / ischemic injury is often unavailable, so that immunohistochemical detection of hsp70 and glial cell staining can be of great value in diagnosing not only the hypoxic / ischemic injury during the process of death but also the victim’s past history of hypoxic attacks. In diffuse axonal injury, degeneration of axon and myelin, such as swelling and waving, were observed in survivors of more than 8 hours. Retraction balls appeared in survivors of more than 1 days. In longer term survivors, such as 3 or 5 months, breakdown of myelin and fat-granule cells were observed. In addition, retraction balls were also found. Immunohistochemical staining of 200 kD neurofilament was a very useful method to examine axonal changes, because antisera is specific for degenerative neurofilaments. In our study, all cases which had pathological findings of diffuse axonal injury (DAI)were associated with focal head injuries. From the immunohistochemical staining of neurons in the hippocampus, it was suggested that neurons in the hippocampus were injured by diffuse brain damage. Furthermore, repairing and protective mechanisms occurred especially from CA2 toCA4. It was considered that neuronal damage in diffuse brain injury was elucidated not only morphologically but also functionally. Therefore, in cases of suspected diffuse brain damage, it is recommended to examine the neuronal changes in addition to observing the findings of diffuse axonal injury. Immunohistochemical staining of the carotid body is potentially very useful for necropsy diagnosis, since it provides a method to detect evidence of mechanical asphyxia in suspected cases of manual and/or ligature strangulation