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Journal articles on the topic 'Minamata disease'

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Published: 10 December 2022
Last updated: 29 January 2023

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1

MURATA, Katsuyuki. "Minamata Disease." TRENDS IN THE SCIENCES 24, no. 10 (October 1, 2019): 10_14–10_17. http://dx.doi.org/10.5363/tits.24.10_14.

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2

Taylor, D. "Minamata disease." Environmental Science & Technology 29, no. 2 (February 1995): 81A. http://dx.doi.org/10.1021/es00002a701.

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3

Eto, Komyo. "Minamata disease." Neuropathology 20, s1 (September 2000): 14–19. http://dx.doi.org/10.1046/j.1440-1789.2000.00295.x.

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4

Semionov, Alexandre. "Minamata Disease—Review." World Journal of Neuroscience 08, no. 02 (2018): 178–84. http://dx.doi.org/10.4236/wjns.2018.82016.

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5

Furuta, Shigeru, Kengo Nishimoto, Masahiko Egawa, Masaru Ohyama, and Hiroyuki Moriyama. "Olfactory Dysfunction in Patients with Minamata Disease." American Journal of Rhinology 8, no. 5 (September 1994): 259–64. http://dx.doi.org/10.2500/105065894782537280.

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We studied the olfactory functions of organic mercury poisoning (Minamata disease) by using both the smell identification test and the olfactory detection threshold test (with phenyl ethyl alcohol). The subjects were 19 patients with Minamata disease who were treated in Meisuien, Minamata, Kumamoto, Japan and include cases that developed the disease in utero. The mean age was 78.7 ± 14.3 years old. Both smell identification and olfactory detection tests in the majority of patients decreased significantly compared with those of healthy elder subjects. A few cases showed normal olfactory identification and detection functions. The olfactory identification function deceased with advancing age. Correlation existed between detection threshold and background factors such as age and duration after documented Minamata disease was found. No significant relationship was identified between olfactory function and the typical symptoms of Minamata disease.
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6

Takaoka, Shigeru. "Minamata Disease at Present." Epidemiology 22 (January 2011): S100. http://dx.doi.org/10.1097/01.ede.0000391973.26704.bc.

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7

Ishihara, Nobuo. "Reconsideration of Minamata disease." Trace Elements and Electrolytes 31, no. 04 (April 1, 2014): 86–88. http://dx.doi.org/10.5414/tex01331.

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8

Smoczyński, Kamil. "Portrety choroby z Minamaty i Niigaty w japońskim filmie dokumentalnym." Studia Filmoznawcze 42 (August 1, 2022): 87–102. http://dx.doi.org/10.19195/0860-116x.42.6.

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The article aims to introduce the history of Japanese documentaries that show the diseases of Minamata and Niigata. To do this, the author initially provides basic information about the origins and symptoms of these diseases. Then the figure of Noriaki Tsuchimoto, a pioneer of portraying Minamata in film, is introduced. The productions Minamata: The Victims and Their World (Minamata: Kanja-san to sono sekai, Japan, 1971) and Shiranui Sea (Shiranuikai, Japan, 1975) are described, which are distinguished by their insightful look into the lives of the people affected by the disease. Another director described in the article is Makoto Satō, whose method the author describes as creative volunteering. Life on the Agano River (Aga ni ikiru, Japan, 1992) focuses on the daily routines of Niigata inhabitants, whose lives were greatly influenced by Satō. Then he created Memories of the Agano River (Aga no kioku, Japan, 2005), which is a documentary experiment with the camera as a medium of memory. The last depicted director is Kazuo Kara, whose Minamata Mandala (Japan, 2020) differs significantly from his earlier works. This production, as stated by the author of the article, aspires to be the last one about the Minamata disease. However, as long as the last patients are fighting for their dignity, the story is not finished.
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9

Takizawa, Y. "Understanding minamata disease and strategies to prevent further environmental contamination by methylmercury." Water Science and Technology 42, no. 7-8 (October 1, 2000): 139–46. http://dx.doi.org/10.2166/wst.2000.0562.

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Minamata disease is a neurological disorder caused by methylmercury poisoning which originated from the discharge of wastewater containing methylmercury from chemical plants in Japan. Residents in the area who consumed large amounts of fish and other seafoods suffered from the disease. The main symptoms consist of sensory disturbance, ataxia, restriction of visual field and hearing impairment. Various measures have been taken to deal with Minamata disease, including environmental pollution control, treatment for patients, and promotion of research activities. Through the compensation law, 2,952 persons have been certified as Minamata disease patients, and a total of approximately 144 billion yen had been paid in compensation by the responsible companies as of March, 1999. Meanwhile, people who were not certified as patients have filed suits against the Japanese Government and local government challenging the diagnostic criteria. The Japanese Government, patients and their supporters reached an agreement in 1996, and Minamata disease legal issues were finally resolved, 40 years after the outbreak. The Minamata experience has left us with an invaluable understanding of the importance of taking thoroughgoing measures to prevent health damage from environmental pollution.
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10

ISHIHARA, Nobuo. "Bibliographical Study of Minamata Disease." Nippon Eiseigaku Zasshi (Japanese Journal of Hygiene) 56, no. 4 (2002): 649–54. http://dx.doi.org/10.1265/jjh.56.649.

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11

Cavanagh, J. B. "THE PATHOLOGY OF MINAMATA DISEASE." Brain 123, no. 1 (January 1, 2000): 195–96. http://dx.doi.org/10.1093/brain/123.1.195.

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12

Funabashi, Harutoshi. "Minamata Disease and Environmental Governance." International Journal of Japanese Sociology 15, no. 1 (November 2006): 7–25. http://dx.doi.org/10.1111/j.1475-6781.2006.00082.x.

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13

ISHIHARA, Nobuo. "Food Sanitation Act and Minamata Disease." Nippon Eiseigaku Zasshi (Japanese Journal of Hygiene) 71, no. 1 (2016): 100–105. http://dx.doi.org/10.1265/jjh.71.100.

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14

Harada, Masazumi, Takashi Yorifuji, and Toshihide Tsuda. "Epidemiology of Congenital Minamata Disease Patients." Epidemiology 22 (January 2011): S100. http://dx.doi.org/10.1097/01.ede.0000391974.64822.d0.

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15

Eto, Komyo. "Review Article: Pathology of Minamata Disease." Toxicologic Pathology 25, no. 6 (November 1997): 614–23. http://dx.doi.org/10.1177/019262339702500612.

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16

TREMBLAY, JEAN-FRANCÇOIS. "Ghisso settles most Minamata disease cases." Chemical & Engineering News 74, no. 23 (June 3, 1996): 8–9. http://dx.doi.org/10.1021/cen-v074n023.p008a.

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17

Takeuchi, Tadao, Takeshi Kambara, Nobuhiro Morikawa, Hideyo Matsumoto, Yukiharu Shiraishi, and Hasuo Ito. "Pathologic Observations of the Minamata Disease**." Pathology International 9 (December 12, 2008): 769–83. http://dx.doi.org/10.1111/j.1440-1827.1959.tb02965.x.

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18

Masazumi, Harada. "Intrauterine Methylmercury Poisoning - Congenital Minamata Disease." Korean Journal of Environmental Health Sciences 33, no. 3 (June 30, 2007): 175–79. http://dx.doi.org/10.5668/jehs.2007.33.3.175.

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19

TAMASHIRO, HIDEHIKO, MIKIO ARAKAKI, HIROKATSU AKAGI, MAKOTO FUTATSUKA, and LEWIS H. ROHT. "Mortality and Survival for Minamata Disease." International Journal of Epidemiology 14, no. 4 (1985): 582–88. http://dx.doi.org/10.1093/ije/14.4.582.

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20

Eto, Komyo, Shinsaku Oyanagi, Yaeko Itai, Hidehiro Tokunaga, Yukio Takizawa, and Ikuo Suda. "A fetal type of Minamata disease." Molecular and Chemical Neuropathology 16, no. 1-2 (February 1992): 171–86. http://dx.doi.org/10.1007/bf03159968.

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21

Matsumoto, S. C., T. Okajima, S. Inayoshi, and H. Ueno. "Minamata disease demonstrated by computed tomography." Neuroradiology 30, no. 1 (February 1988): 42–46. http://dx.doi.org/10.1007/bf00341942.

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22

Yu, Su-jeong. "Disease Disgust Through ‘the Ursprung of Pollution’." Sookmyung Research Institute of Humanities 11 (June 30, 2022): 27–52. http://dx.doi.org/10.37123/th.2022.11.27.

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Disgust is a sensation developed to avoid pathogens. It is developed as an instinct to avoid disease. However, this is limited to ‘disease’. Martha Nussbaum divides aversion into two parts: ‘original disgust’ and ‘projective disgust’. The hatred of the original objects was called ‘original disgust’ and the expansion of people or groups from the original to other objects and considering them as harmful and dangerous ‘pollution sources’ was called ‘projective disgust.’ This study aimed to examine the problem of disease aversion through Ishimure Michiko's novel “Paradise in the Sea of Sorrow” which deals with Japan's representative pollution diseases such as Minamata disease. This text is a monumental work in many ways, including pollution literature, record literature, women's literature, and ecological literature. Through this review, I confirmed in the text how the emotion of “disgust” works within the individual, how it is transferred, and how it expands to group and group to group. What I wanted to reveal through this was the Minamata people as ‘being who is okay to hate’. I think Ishimure would have liked to rewrite the story in Minamata, in “the ursprung” and start again. “Paradise in the Sea of Sorrow” can be established as an “anti-hate novel” that resists stereotypes, prejudice, and discrimination by revealing social stigma and disgust.
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23

KAWAJIRI, Tsuyoshi. "Tentative Assumptions of Historical Research on the “Passing Down of Minamata Disease” by Minamata Disease Sufferers." Japanese Journal of Environmental Education 30, no. 2 (2020): 2_2–13. http://dx.doi.org/10.5647/jsoee.30.2_2.

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24

Kudo, A., Y. Fujikawa, S. Miyahara, J. Zheng, H. Takigami, M. Sugahara, and T. Muramatsu. "Lessons from Minamata mercury pollution, Japan - after a continuous 22 years of observation." Water Science and Technology 38, no. 7 (October 1, 1998): 187–93. http://dx.doi.org/10.2166/wst.1998.0292.

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One of the most visible tragedies by industrial water pollution is Minamata disease, methylmercury poisoning caused by eating contaminated fish, which has killed more than 100 people and paralyzed several thousand people around Minamata Bay, Japan and the adjacent Yatsushiro Sea since 1956. The cause of Minamata disease was confirmed, not by analyzing environmental samples such as sediments (containing more than 600 ppm of Hg) or fish (at least 20 ppm) at the bay, but by symptoms of Minamata disease patients that resembled previous mercury poisoning reported in a European medical journal. Mercury dispersion was traced for 22 years to collect mercury concentration measurements in Yatsushiro Sea surface sediments at 24 fixed stations. The analytical results of mercury revealed four trends of mercury movement from the bay: 1) a rapid increase in Hg concentrations up to 1984; 2) a dramatic decrease in mercury concentrations after an artificial mercury decontamination project began in 1984; 3) a strange drop in mercury contents due to an historical rainfall in the region in 1982 and; 4) natural decontamination, which has been underway since 1985. The tragedy at Minamata has provided many lessons which have shaped the scientific field in environmental research, especially in the area of water quality.
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25

Inoue, Miyo. "The Ethics of Representation in Light of Minamata Disease: Tsuchimoto Noriaki and His Minamata Documentaries." Arts 8, no. 1 (March 20, 2019): 37. http://dx.doi.org/10.3390/arts8010037.

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In this paper, I will examine how Japanese documentary filmmaker Tsuchimoto Noriaki (1928–2008) tackled the issue of visual ethics through the representation of Matsunaga Kumiko and Kamimura Tomoko—two young female patients known for the symbolic roles they each played in the history of Minamata disease. I will introduce the ethical challenge Tsuchimoto encountered upon his first visit to Minamata in 1965—especially how he grappled with the question of filming subjects (shutai) who were unconscious and/or unable to express whether they approved the act of filming or not—and how such conundrums were reflected into his representation of Kumiko in her hospital bed. For the analysis of the representation of Tomoko as seen in Tsuchimoto’s documentary, I will bring in W. Eugene Smith’s photograph “Tomoko and Mother in the Bath” as a point of comparison to explore what could be an ethical representation of Minamata disease patients, including the issue of photographs that seem to beautify the tragedy. Based on the above examinations, I will argue that the challenges Tsuchimoto faced upon representing unresponsive subjects and the very struggle to find a way to capture them as humans, not as patients or victims, altered his manner of artistic and political involvement with Minamata disease. And in the current post-Fukushima era, the issue of ethical representation that he kept exploring carries even more significance upon representing disasters.
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26

Coulter, Margaret A. "Minamata Convention on Mercury." International Legal Materials 55, no. 3 (June 2016): 582–616. http://dx.doi.org/10.5305/intelegamate.55.3.0582.

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This year, 2016, marks the sixtieth anniversary of the discovery of “Minamata Disease,” so-named for the town ravaged by the effects of methylmercury poisoning, and the namesake of the Minamata Convention on Mercury. As of April 22, 2016—Earth Day—128 nations have signed and 25 have ratified the international treaty designed to protect human health and the environment from anthropogenic releases and emission of mercury and mercury compounds.
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27

Sakamoto, Mineshi, Nozomi Tatsuta, Kimiko Izumo, Phuong Phan, Loi Vu, Megumi Yamamoto, Masaaki Nakamura, Kunihiko Nakai, and Katsuyuki Murata. "Health Impacts and Biomarkers of Prenatal Exposure to Methylmercury: Lessons from Minamata, Japan." Toxics 6, no. 3 (August 3, 2018): 45. http://dx.doi.org/10.3390/toxics6030045.

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The main chemical forms of mercury are elemental mercury, inorganic divalent mercury, and methylmercury, which are metabolized in different ways and have differing toxic effects in humans. Among the various chemical forms of mercury, methylmercury is known to be particularly neurotoxic, and was identified as the cause of Minamata disease. It bioaccumulates in fish and shellfish via aquatic food webs, and fish and sea mammals at high trophic levels exhibit high mercury concentrations. Most human methylmercury exposure occurs through seafood consumption. Methylmercury easily penetrates the blood-brain barrier and so can affect the nervous system. Fetuses are known to be at particularly high risk of methylmercury exposure. In this review, we summarize the health effects and exposure assessment of methylmercury as follows: (1) methylmercury toxicity, (2) history and background of Minamata disease, (3) methylmercury pollution in the Minamata area according to analyses of preserved umbilical cords, (4) changes in the sex ratio in Minamata area, (5) neuropathology in fetuses, (6) kinetics of methylmercury in fetuses, (7) exposure assessment in fetuses.
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28

Harada, Masazumi. "Minamata Disease and the Mercury Control Treaty." Material Cycles and Waste Management Research 22, no. 5 (2011): 337–43. http://dx.doi.org/10.3985/mcwmr.22.337.

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29

Yahagi, Tadashi. "CHISSO'S CHANGEOVER TO PETROCHEMICALS AND MINAMATA DISEASE :." Keiei Shigaku (Japan Business History Review) 36, no. 3 (2001): 1–24. http://dx.doi.org/10.5029/bhsj.36.3_1.

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30

SEKI, Reiko. "Social Damage caused by Niigata Minamata Disease." Annual review of sociology 1994, no. 7 (1994): 13–24. http://dx.doi.org/10.5690/kantoh.1994.13.

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31

Kondo, Kiyotaro. "Congenital Minamata Disease: Warnings From Japan's Experience." Journal of Child Neurology 15, no. 7 (July 2000): 458–64. http://dx.doi.org/10.1177/088307380001500707.

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32

POWELL, PAMELA PARADIS. "Minamata Disease: A Story of Mercuryʼs Malevolence." Southern Medical Journal 84, no. 11 (November 1991): 1352–58. http://dx.doi.org/10.1097/00007611-199111000-00014.

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33

Mizukoshi, Kanemasa, Yukio Watanabe, Hideto Kobayashi, Yuuichi Nakano, Chiaki Koide, Shigeki Inomata, and Hisashi Saitoh. "Neurotological Follow-Up Studies upon Minamata Disease." Acta Oto-Laryngologica 108, sup468 (January 1989): 353–57. http://dx.doi.org/10.3109/00016488909139076.

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34

YOSHIDA, Yoshihiro, Hiroshi KAMITSUCHIBASHI, Rikuzo HAMADA, Yoshio KUWANO, Isao MISHIMA, and Akihiro IGATA. "Thuncal Hypesthesia in Patients with Minamata Disease." Internal Medicine 31, no. 2 (1992): 204–7. http://dx.doi.org/10.2169/internalmedicine.31.204.

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35

Igata, A. "Epidemiologic and Clinical Features of Minamata Disease." Environmental Research 63, no. 1 (October 1993): 157–69. http://dx.doi.org/10.1006/enrs.1993.1137.

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36

Fujiki, M., and S. Tajima. "The Pollution of Minamata Bay by Mercury." Water Science and Technology 25, no. 11 (June 1, 1992): 133–40. http://dx.doi.org/10.2166/wst.1992.0284.

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Minamata Disease, methylmercury poisoning, was recognized late in 1953 among the inhabitants living around Minamata Bay. In a chemical factory situated near Minamata Bay, acetaldehyde had been synthesized by the hydration of acetylene till 1968; in the reaction mercury oxide dissolved in sulfuric acid had been used as a catalyst. Inorganic mercury in waste water from the acetaldehyde plant had been discharged into the bay and it had accumulated into bottom sediment. It was proved that a part of inorganic mercury used as the catalyst had changed into methylmercury by a sidereaction in the plant and waste water containing methylmercury from the plant had discharged into the bay and methylmercury had accumulated into the fishes. The mercury concentrations in the muds were very high: in 1963, 29~713 ppm (dry weight); in 1969, 19~908 ppm (dry weight); in 1970, 8~253 ppm (dry weight) and in 1971, 14~586 ppm (dry weight). Since 1977, dredging work had been carried out to remove mercury-contaminated mud and all of the work had finished at March 1990. The concentration of mercury in fishes from the bay was very high in 1959: shellfishes 108~178 ppm (dry weight) and fish 15 ppm (wet weight). Mercury concentration in fishes has decreased markedly since 1966. Total mercury concentration in fishes (87 species) were 0.01~1.74 ppm (wet weight) and fishes containing over 0.4 ppm of total mercury were 16 species in 1989. The hair of patients contained a high concentration of mercury, the highest being 705 ppm. In 1968, the average mercury concentration in patients was 10.6 ppm, for fishermen, the average was 9.2 ppm, and for general inhabitants, the average was 8.1 ppm. In 1982, the average methylmercury concentration in fishermen was 6.15 ppm and for general inhabitants, the averge was 3.78 ppm. Thus, the mercury content in hair decreased gradually with time. After treatment of mercury in waste water was initiated, the mercury content in fishes from Minamta Bay was gradually reduced. It is necessary to supervise strictly to avoid mercury pollution of the environment.
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37

LEE, YUNGJIN. "The Social Life of Disease : A Genealogy of Minamata Disease." Korean Journal of Japanese Dtudies 25 (August 15, 2021): 260–97. http://dx.doi.org/10.29154/ilbi.2021.25.260.

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38

Nomura, Shigeru, and Makoto Futatsuka. "Minamata Disease from the Viewpoint of Occupational Health." Journal of Occupational Health 40, no. 1 (January 1998): 1–8. http://dx.doi.org/10.1539/joh.40.1.

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39

TREMBLAY, JEAN-FRANÇOIS. "Group defies Minamata disease lawsuit settlement in Japan." Chemical & Engineering News 74, no. 13 (March 25, 1996): 21. http://dx.doi.org/10.1021/cen-v074n013.p021.

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40

Itoh, K., Y. Korogi, S. Tomiguchi, M. Takahashi, T. Okajima, and H. Sato. "Cerebellar blood flow in methylmercury poisoning (Minamata disease)." Neuroradiology 43, no. 4 (April 2, 2001): 279–84. http://dx.doi.org/10.1007/s002340000462.

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41

TANNO, Haruka. "Koichi Yanagida and Passing down Activities on Minamata Disease." Japanese Journal of Environmental Education 25, no. 1 (2015): 1_48–59. http://dx.doi.org/10.5647/jsoee.25.1_48.

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42

HARADA, Masazumi. "The global lessons of Minamata Disease-a man's worth." JAPANESE JOURNAL OF LEPROSY 78, no. 1 (2009): 55–60. http://dx.doi.org/10.5025/hansen.78.55.

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43

Yorifuji, Takashi, Tsuguhiko Kato, Yoko Kado, Akiko Tokinobu, Michiyo Yamakawa, Toshihide Tsuda, and Satoshi Sanada. "Intrauterine Exposure to Methylmercury and Neurocognitive Functions: Minamata Disease." Archives of Environmental & Occupational Health 70, no. 5 (June 27, 2014): 297–302. http://dx.doi.org/10.1080/19338244.2014.904268.

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44

Tsuda, Toshihide, and Takashi Yorifuji. "The History of Minamata Disease and Public Health Policy." Epidemiology 22 (January 2011): S99. http://dx.doi.org/10.1097/01.ede.0000391971.19081.05.

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45

Takaoka, Shigeru, Tadashi Fujino, Shinichi Shigeoka, and Yoshinobu Kawakami. "Birth and Onset of Recently Diagnosed Minamata Disease Patients." Epidemiology 22 (January 2011): S298. http://dx.doi.org/10.1097/01.ede.0000392615.41037.d5.

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46

Yorifuji, Takashi, Shigeru Takaoka, and Philippe Grandjean. "Accelerated functional losses in ageing congenital Minamata disease patients." Neurotoxicology and Teratology 69 (September 2018): 49–53. http://dx.doi.org/10.1016/j.ntt.2018.08.001.

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47

Inayosi, S., T. Okajima, S. Matsumoto, and H. Imai. "Short-latency somatosensory evoked potentials (SSEP) in minamata disease." Electroencephalography and Clinical Neurophysiology 75 (January 1990): S64. http://dx.doi.org/10.1016/0013-4694(90)91950-t.

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48

Harada, Masazumi. "Environmental Contamination and Human Rights — Case of Minamata Disease." Industrial & Environmental Crisis Quarterly 8, no. 2 (June 1994): 141–54. http://dx.doi.org/10.1177/108602669400800204.

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49

Nakamura, Masaaki, Masafumi Bekki, Youko Miura, Mina Itatani, and Liu Xiao Jie. "Cerebellar Transcranial Magnetic Stimulation Improves Ataxia in Minamata Disease." Case Reports in Neurology 11, no. 2 (May 8, 2019): 167–72. http://dx.doi.org/10.1159/000500241.

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Minamata disease (MD) is a form of intoxication involving the central nervous system and is caused by ingesting seafood from methylmercury-contaminated areas in Japan. In MD, cerebellar ataxia is a cardinal feature observed in approximately 80% of MD patients. Although cerebellar transcranial magnetic stimulation (TMS) has recently been used for treating cerebellar ataxia, the optimal stimulation conditions remain unclear. Here, we report the first case of cerebellar ataxia in an MD patient that was significantly improved after high-frequency cerebellar TMS. To determine the optimal stimulation conditions, we examined the excitability of the primary motor cortex (M1) using resting-state functional magnetic resonance imaging (rs-fMRI). rs-fMRI revealed M1 hyperconnectivity, which was indicative of activation of the dentato-thalamo-cortical (DTC) pathway. Thus, high-frequency cerebellar TMS was applied to inhibit the DTC pathway. Improvement of cerebellar ataxia was only observed after real TMS, not sham stimulation. As this effect was consistent with inhibition of hyperconnectivity of M1, the effectiveness of high-frequency cerebellar TMS for cerebellar ataxia was thought to be caused by inhibition of the DTC pathway. Therefore, we suggest that the evaluation of M1 excitability using rs-fMRI can be effective for determining the optimal TMS stimulation conditions for cerebellar ataxia.
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50

Albers, Anne, Ursula Gies, Hans-Jurgen Raatschen, and Michael Klintschar. "Another umbrella murder? – A rare case of Minamata disease." Forensic Science, Medicine and Pathology 16, no. 3 (April 22, 2020): 504–9. http://dx.doi.org/10.1007/s12024-020-00247-y.

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