Publications by authors named "Yuichi Miyabara"

There are growing concerns that several aquatic contaminants can indirectly alter biological interactions by inhibiting the adaptive phenotypic plasticity of organisms, even at nonlethal concentrations. In Scenedesmaceae, a family of green algae, many chemicals interfere with defensive colony formation against grazers (i.e.

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In recent decades, lakes have experienced unprecedented ice loss with widespread ramifications for winter ecological processes. The rapid loss of ice, resurgence of winter biology, and proliferation of remote sensing technologies, presents a unique opportunity to integrate disciplines to further understand the broad spatial and temporal patterns in ice loss and its consequences. Here, we summarize ice phenology records for 78 lakes in 12 countries across North America, Europe, and Asia to permit the inclusion and harmonization of in situ ice phenology observations in future interdisciplinary studies.

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A novel comprehensive assessment system, consisting of a bioassay and chemical analysis, was developed to quickly evaluate the human health risk posed by toxic chemicals discharged due to natural disasters. To analyze samples quickly, a yeast-two-hybrid assay (Y2H) and GC-MS equipped with an automated identification and quantification system (AIQS-GC) were employed for the bioassay and chemical analysis, respectively. Since the analysis of 1000 substances by AIQS could be finished within two days following the Y2H assay for screening, this method would complete the risk assessment within three days.

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By mimicking the info-chemicals emitted by grazers, the common anionic surfactant sodium dodecyl sulfate (SDS) can induce colony formation in the green algal genus Scenedesmus at environmentally relevant concentrations. The morphometric effects can hinder the feeding efficiency of grazers, reducing energy flow along the pelagic food chain from Scenedesmus to consumers. Despite this potential ecological risk, few studies exist on whether the SDS-triggered induction of colonies is common in other species of the family Scenedesmaceae.

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Neonicotinoid insecticides that have been on the market since 1992 have been used globally including in Japan. Because they are sprayed over forests and agricultural areas, inadvertent toxicity in nontarget insects (especially honey bees) and humans is a matter of public concern. However, information on exposure levels and potential health impacts of neonicotinoids in children living around sprayed areas is scarce.

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We estimated acute toxicity of benzo[a]pyrene (B[a]P) using two cladoceran species, Ceriodaphnia reticulata and Daphnia magna, and also analyzed its impact on zooplankton community throughout an exposure experiment using small-scale mesocosms. LC(50) of B[a]P for C. reticulata and D.

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We found that aquatic crustaceans, decapoda; atyidae (Caridina multidentata, Neocaridina denticulate, and Paratya compressa), metabolize pyrene to a new conjugation product. The results of deconjugation treatments indicated that glucose and sulfate combined with 1-hydroxypyrene. Further analysis by LC/ESI-MS/MS showed that the molecular weight of the product was 460 (m/z 459; deprotonated ion), and that it has a glucose-sulfate moiety (m/z 241; fragment ion).

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The aquatic crustacean Daphnia magna is an important species for ecotoxicological study, and is often used as a test organism for environmental risk assessment. However, the mechanism of xenobiotic metabolism by this species has not been studied in detail. In the present study, pyrene was used as model substance to investigate the mechanism of xenobiotic metabolism in D.

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To elucidate the historical changes in polychlorinated dibenzo-p-dioxin (PCDD), polychlorinated dibenzofuran (PCDF), coplanar polychlorinated biphenyl (co-PCB), and polycyclic aromatic hydrocarbon (PAH) inflows in Lake Suwa, their concentrations in the sediment core were analyzed in 5 cm interval. The maximum concentrations (depth cm) of PCDDs/DFs, co-PCBs, and PAHs were 25.2 ng/g dry (30-35 cm), 19.

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To determine whether the disruption of thyroid hormone and retinoid homeostasis that occurs after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be mediated by the arylhydrocarbon receptor (AhR), pregnant AhR-heterozygous (AhR+/-) mice were administered a single oral dose of 10 microg kg(-1) TCDD at gestation day 12.5. Serum and liver were collected on postnatal day 21 from vehicle-treated control or TCDD-treated AhR+/- and AhR-null (AhR-/-) mouse pups.

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This article reports the organ distribution and bioaccumulation of hepatotoxic microcystins (MCs) in freshwater fishes at different trophic levels from the large, shallow, eutrophic Lake Chaohu in September 2003, when there were heavy surface blooms of toxic cyanobacteria. Among all fish, intestines and blood had the highest average content of MC-RR + MC-LR (22.0 and 14.

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Objectives: To clarify the origin of dioxin and related compounds (dioxins) in human hair, we determined the amounts of adsorbed dioxins in human hair, and the distribution of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rats.

Methods: Human hair specimens, packed in a glass column, were exposed to ambient air that was introduced into the column with an air pump for 24 h. Rats were administered TCDD by gavage at doses of 0.

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Dioxin-like polychlorinated biphenyls (PCBs) exert their toxicities by activating the arylhydrocarbon receptor (AhR), a ligand-dependent transcription factor, in a similar manner to the most toxic dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In the present study, we re-evaluated the relative potency (REP) of the toxic members of dioxin-like PCBs, PCB126 (toxic equivalency factor, TEF 0.1) and PCB169 (TEF 0.

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Dioxin and its related compounds are suspected to cause neurological and nueroendocrinological disruption in human and laboratory animal offspring upon in utero and lactational exposure during growth and development. We tested the hypothesis by utilizing Long-Evans Hooded rats that perinatal exposure to dioxins affects the neocortical function and expression of sexual behavior in adulthood. In the sexual behavior test, perinatal exposure to TCDD significantly reduced the number of mounts and intromissions.

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The present study was conducted to clarify the involvement of mast cells in the exacerbating effect of diesel exhaust particles (DEP) toward allergic airway inflammation and airway hyperresponsiveness (AHR). Airway inflammation by the infiltration of cosinophils with goblet cell proliferation and AHR, as well as by the production of antigen-specific IgG1 and IgE, in plasma were examined using mast cell-deficient mice (W/W(v)) and normal mice (W/W(+)). Both groups of mice received ovalbumin (OVA) or OVA+DEP intratracheally.

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Concentrations of polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs) and coplanar biphenyls (Co-PCBs) were determined in Japanese human adipose tissues. Temporal trends were assessed by comparing data collected during 1970-1971, 1994-1996 and 2000. Mean TEQ levels of PCDD/Fs in human adipose tissue showed a significant decrease from 31.

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Exposure to a relatively low dose of 2,3,7,8-tetrachlorodebenzo-p-dioxin (TCDD) during mid-gestation induces a reduction of ventral prostate weight in rat offspring. Recently we reported that a single administration of TCDD (12.5-800 ng/kg body weight) to pregnant Holtzman rats on gestational day (GD) 15 caused a decrease in androgen receptor (AR) mRNA level in the ventral prostate during the prepubertal period, and we proposed that this reduction of AR mRNA is one of the most sensitive adverse endpoints due to perinatal exposure to TCDD (S.

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Exposure to a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produces a variety of toxic manifestations, including fetal death. In order to evaluate the effects of low-dose TCDD on placental function in this study, pregnant Holtzman rats were given a single oral dose of 800 or 1600 ng TCDD/kg body wt or an equivalent volume of vehicle (control) on gestation day (GD) 15 and the results were observed on GD16 and GD20. The number of fetal deaths increased in the animals exposed to TCDD.

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We have investigated how a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects thyroid hormone regulation, especially in relation to the localization of thyroid stimulating hormone (TSH) in the pituitary and that of thyroxin (T4) of the thyroid in the rat. Female Sprague-Dawley rats were given a single oral administration of TCDD ranging from 1.0 to 4.

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