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

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

One autopsy case of cyanide-gas poisoning

A fishing-boat was smoked with cyanide-gas to rid vermin. A thirty-year old male was found dead in a cabin of the boat. Autopsy revealed fluid blood, and petechial haemorrhage in conjunctivas, thymus, heart and lungs. Lung, spleen, kidney and other organs were strongly congested. Bleedings in sternocleidomastoideus and sterunohyoideus muscles were found. The bloody foam and solution were also observed in trachea. From these autopsy findings, it was considered that he failed into severe dyspnea. Furthermore, postmortem lividity was bright pink color and the left cardiac blood was also bright pink, so there was markly different between the color of right and left cardiac blood. To make clear his cause of death, during the autopsy the screening test of cyanide, Schonbein-Pagenstecher method, was tried and then it was positive. Further toxicological analysis, quantitative measurement revealed 6.25 μg/ml of cyanide from his blood. From the results of autopsy and toxicological findings, his cause of death was diagnosed as the cyanide-gas poisoning

HSP70 and c-Fos expression of brain stem hypoglossal nucleus in drowning

The brain stem hypoglossal nucleus (HN) is the center of nerves innervating the upper respiratory tract and is related to control of mastication, deglutition, speech and respiration. To elucidate the relationship between asphyxia and the HN, we investigated the change of hypoglossal neurons in cases of hanging, strangulation, smothering, choking, drowning and respiratory failure. Using immunohistochemical techniques, we observed the brain stem HN with antibodies against microtubule-associated protein2(MAP2), muscarinic acetylcholine receptor (mAChR), c-fos gene product (c-Fos) and 72kD heat-shock protein (HSP70). MAP2, a cytoskeletal protein of the neuron, is a marker of neuronal damage. Muscarinic AChR was used as a marker of neuronal membrane and ACh signaling. We employed both HSP70 and c-Fos as markers of stress- or damage-related events. We measured the percentage of immunopositive neurons in total neurons of HN. Drowning produced higher expression of HSP70 and c-Fos than other causes of asphyxia, suggesting that drowning induces more severe damage in HN neurons. Furthermore, it was suspected that neuronal changes in drowning might relate to functions of the HN. These observations indicate that immunohistochemical examination of the brain stem HN could provide useful information for determining the cause of asphyxia

ゲンパツセイ コウジョウセンガン ノ ネンレイ ニヨル リンショウ ビョウリガクテキ トクチョウ オヨビ ヨゴ ノ ヒカク ケントウ

Two-hundred thirty-six patients with primary thyroid cancer who received operation were divided into two groups by age, i.e.,５９patients of age ＜４５years（Early adulthood, EA）and１７７ patients of age≧４５years（advanced age, AA）. Clinicopathologic factors and disease-free survival （DFS）were compared between the two groups. There was no difference in clinicopathologic factors except for higher proportion of patients with poorly differentiated adenocarcinoma in the AA patients than in the EA patients（６．７％ vs. ０％, p＝０．０４１）. DFS was significantly longer in the AA patients than in the EA patients（disease-free rates at１０years after operation，９４．８％ vs. ７２．５％, p＝０．００３１）. Overall survival was not different between the two groups. The EA patients who showed shorten DFS were divided into two groups，１７ patients of age ＜３０ years （juvenile and young adult, JYA）and ４２ patients of age ≧３０ years, and DFS of each group was compared with that of the AA patients. Although disease-free survival rates at １０ years of the JYA patients were not different（９２．６％ vs.９４．８％, p＝０．１２５）, those of patients of age ≧３０years were significantly lower than those of the AA patients（７０．０％ vs. ９４．８％, p＝０．００２１）. These findings suggest that patients with primary thyroid cancer who are ≧３０ years old in the young adulthood should be observed carefully after operation for early detection of relapse

Parkinson’s disease-associated iPLA2-VIA/PLA2G6 regulates neuronal functions and α-synuclein stability through membrane remodeling

Mutations in the iPLA2-VIA/PLA2G6 gene are responsible for PARK14-linked Parkinson’s disease (PD) with α-synucleinopathy. However, it is unclear how iPLA2-VIA mutations lead to α-synuclein (α-Syn) aggregation and dopaminergic (DA) neurodegeneration. Here, we report that iPLA2-VIA–deficient Drosophila exhibits defects in neurotransmission during early developmental stages and progressive cell loss throughout the brain, including degeneration of the DA neurons. Lipid analysis of brain tissues reveals that the acyl-chain length of phospholipids is shortened by iPLA2-VIA loss, which causes endoplasmic reticulum (ER) stress through membrane lipid disequilibrium. The introduction of wild-type human iPLA2-VIA or the mitochondria–ER contact site-resident protein C19orf12 in iPLA2-VIA–deficient flies rescues the phenotypes associated with altered lipid composition, ER stress, and DA neurodegeneration, whereas the introduction of a disease-associated missense mutant, iPLA2-VIA A80T, fails to suppress these phenotypes. The acceleration of α-Syn aggregation by iPLA2-VIA loss is suppressed by the administration of linoleic acid, correcting the brain lipid composition. Our findings suggest that membrane remodeling by iPLA2-VIA is required for the survival of DA neurons and α-Syn stability

Acute urinary retention in a 23-year-old woman with mild encephalopathy with a reversible splenial lesion: a case report

<p>Abstract</p> <p>Introduction</p> <p>Patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion present with relatively mild central nervous system disturbances. Although the exact etiology of the condition remains poorly understood, it is thought to be associated with infective agents. We present a case of a patient with mild encephalitis/encephalopathy with a reversible splenial lesion, who had the unusual feature of acute urinary retention.</p> <p>Case presentation</p> <p>A 23-year-old Japanese woman developed mild confusion, gait ataxia, and urinary retention seven days after onset of fever and headache. Magnetic resonance imaging demonstrated T2 prolongation in the splenium of the corpus callosum and bilateral cerebral white matter. These magnetic resonance imaging abnormalities disappeared two weeks later, and all of the symptoms resolved completely within four weeks. Except for the presence of acute urinary retention (due to underactive detrusor without hyper-reflexia), the clinical and radiologic features of our patient were consistent with those of previously reported patients with mild encephalitis/encephalopathy with a reversible splenial lesion. To the best of our knowledge, this is the first report of acute urinary retention recognized in a patient with mild encephalitis/encephalopathy with a reversible splenial lesion.</p> <p>Conclusion</p> <p>Our findings suggest that mild encephalitis/encephalopathy with a reversible splenial lesion can be associated with impaired bladder function and indicate that acute urinary retention in this benign disorder should be treated immediately to avoid bladder injury.</p