285 results match your criteria: "National Institute for Minamata Disease[Affiliation]"

Article Synopsis
  • Minamata disease is a severe neurological disorder caused by methylmercury (MeHg) poisoning, identified in Japan in 1956, and previously thought to be linked to elevated selenium (Se) levels in patients.
  • Research showed both mercury and selenium were present in historical samples from Minamata Bay, indicating that Se also contaminated the area and accumulated in patients' organs.
  • The study's findings, including high Hg/Se molar ratios in brain tissue, help explain the neurological damage seen in patients and emphasize the dangers of consuming MeHg-contaminated seafood.
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Article Synopsis
  • The study aimed to investigate why pregnant women with glucose intolerance often have large infants, focusing on amino and fatty acid transport in the placenta, beyond just glucose transport.
  • Researchers analyzed postpartum placental tissues from 101 eligible deliveries, finding higher expression levels of certain transporters (LAT1 and placenta-FABPpm) in women with glucose intolerance compared to those without.
  • The results suggest that, despite controlled blood sugar levels, managing other nutrients like amino acids and fatty acids in glucose-intolerant pregnancies is crucial for fetal growth.
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Therapeutic potential of 4-phenylbutyric acid against methylmercury-induced neuronal cell death in mice.

Arch Toxicol

October 2024

Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700‑8530, Japan.

Methylmercury (MeHg) is an environmental neurotoxin that induces damage to the central nervous system and is the causative agent in Minamata disease. The mechanisms underlying MeHg neurotoxicity remain largely unknown, and there is a need for effective therapeutic agents, such as those that target MeHg-induced endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), which is activated as a defense mechanism. We investigated whether intraperitoneal administration of the chemical chaperone, 4-phenylbutyric acid (4-PBA), at 120 mg/kg/day can alleviate neurotoxicity in the brains of mice administered 50 ppm MeHg in drinking water for 5 weeks.

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Electronic waste (e-waste) contains hazardous elements such as lead (Pb), cadmium (Cd), mercury (Hg), and other toxic elements that pose significant health risks to the population directly exposed. We recruited 199 e-waste recycling workers and 104 non-exposed workers in Bangladesh and analyzed heavy metals in blood and hair, as well as hematological and cardiovascular parameters including, blood lipids and blood pressure. We fitted quantile regression models at 0.

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Development of a sensor to detect methylmercury toxicity.

Sci Rep

September 2024

Department of Basic Medical Sciences, National Institute for Minamata Disease, 4058-18 Hama, Minamata, Kumamoto, 867-0008, Japan.

Methylmercury (MeHg) is a well-known neurotoxicant that induces various cellular functions depending on cellular- and developmental-specific vulnerabilities. MeHg has a high affinity for selenol and thiol groups, thus impairing the antioxidant system. Such affinity characteristics of MeHg led us to develop sensor vectors to assess MeHg toxicity.

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Methylmercury (MeHg) is an environmental toxin known to damage the central nervous system. When pregnant women ingest seafood, which may contain accumulated MeHg, fetal development may be affected. The embryonic period, a time of major epigenetic change, is susceptible to epigenetic disruptions due to chemical exposure.

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Methylmercury (MeHg) is widely distributed in nature and is known to cause neurotoxic effects. This study aimed to examine the anti-MeHg activity of oleanolic acid-3-glucoside (OA3Glu), a synthetic oleanane-type saponin derivative, by evaluating its effects on motor function, pathology, and electrophysiological properties in a mouse model of MeHg poisoning. Mice were orally administered 2 or 4 mg·kg·d MeHg with or without 100 µg·kg·d OA3Glu 5x/week for four weeks.

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Article Synopsis
  • Methylmercury (MeHg) causes significant damage to the nervous system, leading to symptoms like sensory disturbances and neuropathic pain in chronic Minamata disease patients.
  • Gabapentin was tested on Minamata disease model rats to see if it could alleviate neuropathic pain, with analyses conducted on the nervous system to understand its effects.
  • The study found that while gabapentin did not reverse neurodegeneration or microglial activation, it appeared to reduce synaptic rewiring in the somatosensory cortex, suggesting it may help manage neuropathic pain related to MeHg poisoning.
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Electronic waste (e-waste) contains numerous metals and organic pollutants that have detrimental impacts on human health. We studied 199 e-waste recycling workers and 104 non-exposed workers; analyzed blood, urine, and hair samples to measure heavy metals, hormonal, liver, and renal function. We used quantile regression models to evaluate the impact of Pb, Cd, and Hg on hormonal, liver and renal function, and the role of DNA oxidative damage in mediating the relationship between exposures and outcomes.

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Background: Electronic waste (e-waste) recycling activities release toxic metals, which pose substantial hazard to the environment and human health. We evaluated metal concentrations in biological and environmental samples, and examined the associations between biological lead (Pb), cadmium (Cd), and mercury (Hg) with soil and dust metals, and other possible determinants, among populations exposed and non-exposed to e-waste in Bangladesh.

Methods: A total of 199 e-waste workers and 104 non-exposed individuals were recruited.

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Characterization of pathological changes in the olfactory system of mice exposed to methylmercury.

Arch Toxicol

April 2024

Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700‑8530, Japan.

Methylmercury (MeHg) is a well-known environmental neurotoxicant that causes severe brain disorders such as Minamata disease. Although some patients with Minamata disease develop olfactory dysfunction, the underlying pathomechanism is largely unknown. We examined the effects of MeHg on the olfactory system using a model of MeHg poisoning in which mice were administered 30 ppm MeHg in drinking water for 8 weeks.

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Methylmercury (MeHg) causes selective neuronal damage to cerebrocortical neurons (CCNs) in the central nervous system, but not to hippocampal neurons (HiNs), which are highly vulnerable to neurodegenerative diseases. In our previous study using cultured rat neurons, we performed a comprehensive gene expression analysis and found that the brain-derived neurotrophic factor (BDNF), a neurotrophin (NT), was specifically expressed in HiNs. Therefore, to elucidate the causal factors of MeHg toxicity resistance in HiNs, we conducted a comparative study of the protein expression and function of several NTs, including BDNF, using CCNs showing vulnerability to MeHg toxicity and HiNs showing resistance.

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Methylmercury-induced brain neuronal death in CHOP-knockout mice.

J Toxicol Sci

February 2024

Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University.

Apoptosis is one of the hallmarks of MeHg-induced neuronal cell death; however, its molecular mechanism remains unclear. We previously reported that MeHg exposure induces neuron-specific ER stress in the mouse brain. Excessive ER stress contributes to apoptosis, and CHOP induction is considered to be one of the major mechanisms.

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We analyzed total mercury content (THg) and carbon (δC) and nitrogen (δN) stable isotope ratios in fish, subtidal macrobenthos, and particulate organic matter (POM) as a proxy for pelagic phytoplankton and attached microalgae as a proxy for microphytobenthos to investigate the mercury exposure pathway in fish. For four seasons, samples of the above-mentioned organisms were collected on five occasions (July and October 2018 and January, April, and July 2019) in Minamata Bay. Isotope analysis showed that Minamata Bay food web structures were almost entirely fueled by microphytobenthos.

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Maternal DHA intake in mice increased DHA metabolites in the pup brain and ameliorated MeHg-induced behavioral disorder.

J Lipid Res

November 2023

Program of Life and Environmental Sciences, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.

Although pregnant women's fish consumption is beneficial for the brain development of the fetus due to the DHA in fish, seafood also contains methylmercury (MeHg), which adversely affects fetal brain development. Epidemiological studies suggest that high DHA levels in pregnant women's sera may protect the fetal brain from MeHg-induced neurotoxicity, but the underlying mechanism is unknown. Our earlier study revealed that DHA and its metabolite 19,20-dihydroxydocosapentaenoic acid (19,20-DHDP) produced by cytochrome P450s (P450s) and soluble epoxide hydrolase (sEH) can suppress MeHg-induced cytotoxicity in mouse primary neuronal cells.

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Background: Fish are a rich source of essential nutrients that protect against preterm birth. However, as fish can absorb environmental pollutants, their consumption can also increase the risk of preterm birth. This study aimed to assess whether maternal fish consumption during pregnancy is associated with preterm birth in a nationwide large Japanese cohort that consumed relatively high amounts and many types of fish.

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The most severe effects of methylmercury (MeHg) exposure during child development are thought to result from exposure during fetal life and childhood. However, comparing the neurodevelopmental effects of prenatal and postnatal MeHg exposure (PreMeHg and PostMeHg, respectively) remains unclear. We aimed to investigate the associations between neurodevelopmental indicators and PreMeHg or PostMeHg.

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Granule cell-selective toxicity of methylmercury in the cerebellum is one of the main unresolved issues in the pathogenesis of Minamata disease. Rats were orally administered methylmercury chloride (10 mg/kg/day) for 5 consecutive days, and their brains were harvested on days 1, 7, 14, 21, or 28 after the last administration for histological examination of the cerebellum. It was found that methylmercury caused a marked degenerative change to the granule cell layers but not to the Purkinje cell layers.

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Methylmercury pollution is a global problem, and Minamata disease (MD) is a stark reminder that exposure to methylmercury can cause irreversible neurological damage. A "glove and stocking type" sensory disturbance due to injured primary sensory cortex (SI) (central somatosensory disturbance) is the most common neurologic sign in MD. As this sign is also prevalent in those with polyneuropathy, we aimed to develop an objective assessment for detecting central somatosensory disturbances in cases of chronic MD.

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Objectives: The mask fit test confirms whether the wearing condition of the wearer's face and the facepiece of the respirators are used appropriately. This study aimed to examine whether the results of the mask fit test affect the association between the concentration of metals related to welding fumes in biological samples and the results of time-weighted average (TWA) personal exposures.

Methods: A total of 94 male welders were recruited.

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Objectives: There are some studies reporting the association between (manganese [Mn]) exposure to welding fume and neurological dysfunction. This study examined the relationship between Mn exposure and neurological behavior in Japanese male welders and non-welders using biological samples, which to date has not been assessed in Japan.

Methods: A total of 94 male welders and 95 male non-welders who worked in the same factories were recruited.

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Polycyclic aromatic hydrocarbons in urban particle matter exacerbate movement disorder after ischemic stroke via potentiation of neuroinflammation.

Part Fibre Toxicol

February 2023

Program of Biomedical Science, Graduate School of Integrated Sciences for Life, Hiroshima University, 1-7-1, Kagamiyama, Higashi-Hiroshima, Hiroshima, 739-8521, Japan.

Background: A recent epidemiological study showed that air pollution is closely involved in the prognosis of ischemic stroke. We and others have reported that microglial activation in ischemic stroke plays an important role in neuronal damage. In this study, we investigated the effects of urban aerosol exposure on neuroinflammation and the prognosis of ischemic stroke using a mouse photothrombotic model.

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Mercury (Hg) is a chemical of health concern worldwide that is now being acted upon through the Minamata Convention. Operationalizing the Convention and tracking its effectiveness requires empathy of the diversity and variation of mercury exposure and risk in populations worldwide. As part of the health plenary for the 15th International Conference on Mercury as a Global Pollutant (ICMGP), this review paper details how scientific understandings have evolved over time, from tragic poisoning events in the mid-twentieth century to important epidemiological studies in the late-twentieth century in the Seychelles and Faroe Islands, the Arctic and Amazon.

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Relationship between grave visitation and apathy among community-dwelling older adults.

Psychogeriatrics

May 2023

Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.

Background: It has been shown that involvement in religious activities has a positive impact on psychological aspects. In this study, the relationship between grave visitation, a standard religious activity in Japan, and depression and apathy symptoms was investigated among older adults in Japan.

Methods: A total of 638 older adults who participated in a community-based health check survey (Tarumizu Study 2019) were interviewed regarding the presence or absence of grave visitation, frequency, travel time, means of transportation, and flower offerings.

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Exploratory whole-brain studies in patients suffering from methylmercury (MeHg) poisoning have not been conducted. We aimed to evaluate the neuroanatomical differences between patients with chronic MeHg poisoning and healthy volunteers via magnetic resonance (MR) imaging. Patients included in this case-control study were divided into three categories based on whether MeHg exposure occurred in utero, under 15 years of age, or over 15 years of age, as fetal-, pediatric-, and adult-type patients, respectively.

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