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Biomedical subjects

H Tokunaga

Publications and source records attributed to H Tokunaga.

209 records · Page 12Linked to original sources
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A fetal type of Minamata disease. An autopsy case report with special reference to the nervous system.

Our knowledge concerning the pathology of fetal cases of human Minamata disease (methylmercury poisoning) is relatively limited. We report here a case with description of the distribution of mercury in the systemic organs, and the ultrastructural changes of the nervous system after a survival of 29 yr. The patient was a female born in 1957, with a body wt of 3000 g, who died in 1987. She carried a diagnosis of cerebral palsy, and had a convulsion at age 3 yr. Mercury levels in her mother's hair were 101 micrograms/g at the time of examination in 1959. At autopsy, the body measured 43 cm and weighed 23 kg. The brain weighed 920 g and showed marked cerebral atrophy, mild neuronal loss in the calcarine, postcentral and precentral cortices, cerebellar atrophy, and segmental demyelination of peripheral nerves. Mercury granules were present in the brain, kidney, and liver. Ultrastructural examination of the calcarine, post- and precentral cortices, and cerebellar cortices, showed severe atrophy of nerve cells, with a decrease in rough ER and an increase in nuclear chromatin and preservation of mitochondria. Autophagosomes were increased in number. In addition, high electron density, globular and dense bodies, measuring 0.3-1.8 microns in diameter, were found, surrounded by limited membrane, within both cerebral and cerebellar neurons. In the cellebellum, synapses were well-preserved.

Adult↗
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Methylmercury poisoning in common marmosets--a study of selective vulnerability within the cerebral cortex.

Neuropathological lesions found in chronic human Minamata disease tend to be localized in the calcarine cortex of occipital lobes, the pre- and postcentral lobuli, and the temporal gyri. The mechanism for the selective vulnerability is still not clear, though several hypotheses have been proposed. One hypothesis is vascular and postulates that the lesions are the result of ischemia secondary to compression of sulcal arteries from methylmercury-induced cerebral edema. To test this hypothesis, we studied common marmosets because the cerebrum of marmosets has 2 distinct deep sulci, the calcarine and Sylvian fissures. MRI analysis, mercury assays of tissue specimens, histologic and histochemical studies of the brain are reported and discussed. Brains sacrificed early after exposure to methylmercury showed high contents of methylmercury and edema of the cerebral white matter. These results may explain the selective cortical degeneration along the deep cerebral fissures or sulci.

Animals↗
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Neuropathological analysis of dementia in a Japanese leprosarium.

In a neuropathological study of consecutive autopsies, prevalence and cause of dementia in a Japanese leprosarium were investigated, where more than 95% of inpatients with a mean age of 70 years are now free from active leprosy. In 10 years (1983-1992), clinically overt dementia at death was 35/136 (25.7%) in the age group over 65 years (mean age 79.4). Autopsy was performed in 85 cases (mean age 81 years), and clinically overt dementia was seen in 25 subjects (29.4%). Neuropathologically, Alzheimer's disease (AD) was seen in 9 cases (10.6%), vascular dementia (VD) in 9 cases (10.6%), mixed type in 3 cases (3.5%) and unclassified in 4 cases (4.7%). In the age group of 65-84 years, AD was 5/58 (8.6%), VD was 4/58 (6.9%), mixed type was 2/58 (3.4%), and unclassified was 1/58 (1.7%). Compared with previous Japanese general population-based data, where VD was more frequent than AD, the rate of dementia in our leprosarium was high, and pathologically confirmed AD was as common as VD. Recently, a prophylactic effect of the antileprosy and anti-inflammatory drug DDS (dapsone, 4,4'-diaminodiphenyl sulfone) has been suggested. Lepromatous patients take more DDS (51.9%) than tuberculoid patients (11.5%), however, as the dementia rate of tuberculoid leprosy (17.9%) in those 65-84 years old is similar to lepromatous leprosy (15.9%) in our study, we do not support their viewpoint.

Age Factors↗
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Expression of cytokines on human bronchial epithelial cells induced by influenza virus A.

Bronchial epithelial cells play an important role in the pathogenesis of some inflammatory diseases of bronchial mucosa. Epithelial-cell-derived cytokines are important in the elucidation of the mechanism by which airway inflammation occurs, especially in respiratory virus infection, because these cells are the primary sites of viral infection. We infected bronchial epithelial cells, NCI-H292, with influenza virus A (H3N2) and examined the concentrations of cytokines, interleukin-6 (IL-6), IL-8 and regulated on activation, normal T cells, expressed and secreted (RANTES), in the culture media of infected cells using the enzyme-linked immunosorbent assay system and gene expression of RANTES on epithelial cells by the reverse-transcriptase-polymerase chain reaction method. We found that significant amounts of IL-6, IL-8 and RANTES were released. RANTES mRNA was also detected in infected bronchial epithelial cells. It is suggested that cytokine production in human bronchial epithelial cells may contribute to the pathogenesis of airway inflammatory disorders.

Bronchi↗
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Differential diagnosis between organic and inorganic mercury poisoning in human cases--the pathologic point of view.

Differences in pathology were found between acute and chronic exposure to methylmercury, mercury vapor, and inorganic mercury. Characteristic pathologic changes produced by organic mercury in the brain have previously been described in patients with Minamata disease. The brains of patients who presented with acute onset of symptoms and died within 2-mo showed loss of neurons with reactive proliferation of glial cells, microcavitation, vascular congestion, petechial hemorrhage, and edema in the cerebral cortices, predominantly in the calcarine, pre- and postcentral, and transverse temporal cortices and in the cerebellar cortex. The neuropathologic changes in the patients with acute onset of symptoms who survived for a long period (>10 yr) were also included neuronal loss with reactive proliferation of glial cells in similar anatomic locations. The neuropathologic changes in patients with inorganic mercury poisoning are quite different. Autopsies performed on 3 individuals with fatal cases of acute inorganic mercury poisoning who were exposed to mercury vapor for about 2 wk revealed diffuse organized pneumonia, renal cortical necrosis, disseminated intravascular coagulopathy, and infarctions in the brain and kidneys. In 2 other patients who worked in mercury mines for about 10 yr and who suffered from chronic inorganic poisoning, no specific lesions were demonstrated in the brain. However, the assay and the histochemistry of mercury revealed that inorganic mercury was present in the brain in all 3 groups irrespective of the brain lesions and the duration of clinical signs.

Adult↗
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Multiple parapapillary choledochoduodenal fistulas with ampullary carcinoma.

Only very rarely do multiple parapapillary choledochoduodenal fistulas occur concurrently with ampullary carcinoma. The following presents just such a case, which occurred in a 51 year-old Japanese female hospitalized for epigastralgia. Gastrointestinal fiberscopy (GIF) showed abnormal swelling of Vater's papilla. She was diagnosed as having ampullary carcinoma and choledochoduodenal fistulas, as determined by hypotonic duodenography (HDG), endoscopic retrograde cholangiopancreatography (ERCP) and from the histopathology of the ampullary mucosal biopsy. Pancreatoduodenectomy was performed. We postulated that the multiple fistulas were formed on the longitudinal fold of Vater's papilla by an ampullary carcinoma, and that the fistulas played a major role in bile drainage. As a result, jaundice was not seen throughout the entire clinical course. We report on the mechanism of fistula formation, with a review of the recent literature.

Ampulla of Vater↗