105 research outputs found

    Relationship between Environmental Phthalate Exposure and the Intelligence of School-Age Children

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    BACKGROUND: Concern over phthalates has emerged because of their potential toxicity to humans. OBJECTIVE: We investigated the relationship between the urinary concentrations of phthalate metabolites and children`s intellectual functioning. METHODS: This study enrolled 667 children at nine elementary schools in five South Korean cities. A cross-sectional examination of urine phthalate concentrations was performed, and scores on neuro-psychological tests were obtained from both the children and their mothers. RESULTS: We measured mono-2-ethylhexyl phthalate (MEHP) and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), both metabolites of di(2-ethylhexyl)phthalate (DEHP), and mono-n-butyl phthalate (MBP), a metabolite of dibutyl phthalate (DBP), in urine samples. The geometric mean (ln) concentrations of MEHP, MEOHP, and MBP were 21.3 mu g/L [geometric SD (GSD) = 2.2 mu g/L; range, 0.5-445.4], 18.0 mu g/L (GSD = 2.4; range, 0.07-291.1), and 48.9 mu g/L (GSD = 2.2; range, 2.1-1645.5), respectively. After adjusting for demographic and developmental covariates, the Full Scale IQ and Verbal IQ scores were negatively associated with DEHP metabolites but not with DBP metabolites. We also found a significant negative relationship between the urine concentrations of the metabolites of DEHP and DBP and children`s vocabulary subscores. After controlling for maternal IQ, a significant inverse relationship between DEHP metabolites and vocabulary subscale score remained. Among boys, we found a negative association between increasing MEHP phthalate concentrations and the sum of DEHP metabolite concentrations and Wechsler Intelligence Scale for Children vocabulary score; however, among girls, we found no significant association between these variables. CONCLUSION: Controlling for maternal IQ and other covariates, the results show an inverse relationship between phthalate metabolites and IQ scores; however, given the limitations in cross-sectional epidemiology, prospective studies are needed to fully explore these associations.This work was funded by the Eco-Technopia 21 project of Korea Institute of Environmental Science and Technology (091-081-059).Cho SC, 2010, J CHILD PSYCHOL PSYC, V51, P1050, DOI 10.1111/j.1469-7610.2010.02250.xKim BN, 2009, BIOL PSYCHIAT, V66, P958, DOI 10.1016/j.biopsych.2009.07.034Tanida T, 2009, TOXICOL LETT, V189, P40, DOI 10.1016/j.toxlet.2009.04.005Ghisari M, 2009, TOXICOL LETT, V189, P67, DOI 10.1016/j.toxlet.2009.05.004Barnett JH, 2009, AM J PSYCHIAT, V166, P909, DOI 10.1176/appi.ajp.2009.08081251Kim Y, 2009, NEUROTOXICOLOGY, V30, P564, DOI 10.1016/j.neuro.2009.03.012Engel SM, 2009, NEUROTOXICOLOGY, V30, P522, DOI 10.1016/j.neuro.2009.04.001Kamrin MA, 2009, J TOXICOL ENV HEAL B, V12, P157, DOI 10.1080/10937400902729226Brown JS, 2009, SCHIZOPHRENIA BULL, V35, P256, DOI 10.1093/schbul/sbm147Bellinger DC, 2008, NEUROTOXICOLOGY, V29, P828, DOI 10.1016/j.neuro.2008.04.005Wolff MS, 2008, ENVIRON HEALTH PERSP, V116, P1092, DOI 10.1289/ehp.11007van Neerven S, 2008, PROG NEUROBIOL, V85, P433, DOI 10.1016/j.pneurobio.2008.04.006Hatch EE, 2008, ENVIRON HEALTH-GLOB, V7, DOI 10.1186/1476-069X-7-27Zevalkink J, 2008, J GENET PSYCHOL, V169, P72Kolarik B, 2008, ENVIRON HEALTH PERSP, V116, P98, DOI 10.1289/ehp.10498SATHYANARAYANA S, 2008, CURR PROBL PEDIAT AD, V38, P34KHO YL, 2008, J ENV HLTH SCI, V34, P271Huang PC, 2007, HUM REPROD, V22, P2715, DOI 10.1093/humrep/dem205Janjua NR, 2007, ENVIRON SCI TECHNOL, V41, P5564, DOI 10.1021/es0628755Meeker JD, 2007, ENVIRON HEALTH PERSP, V115, P1029, DOI 10.1289/ehp.9852Fromme H, 2007, INT J HYG ENVIR HEAL, V210, P21, DOI 10.1016/j.ijheh.2006.09.005Xu Y, 2007, ARCH TOXICOL, V81, P57, DOI 10.1007/s00204-006-0143-8Pereira C, 2007, ACTA HISTOCHEM, V109, P29, DOI 10.1016/j.acthis.2006.09.008Hauser R, 2006, EPIDEMIOLOGY, V17, P682, DOI 10.1097/01.ede.0000235996.89953.d7Zhu DF, 2006, BRAIN, V129, P2923, DOI 10.1093/brain/awl215Andrade AJM, 2006, TOXICOLOGY, V227, P185, DOI 10.1016/j.tox.2006.07.022Lottrup G, 2006, INT J ANDROL, V29, P172, DOI 10.1111/j.1365-2605.2005.00642.xBreous E, 2005, MOL CELL ENDOCRINOL, V244, P75, DOI 10.1016/j.mce.2005.06.009Wenzel A, 2005, MOL CELL ENDOCRINOL, V244, P63, DOI 10.1016/j.mce.2005.02.008Kato K, 2005, ANAL CHEM, V77, P2985, DOI 10.1021/ac0481248Tanaka T, 2005, FOOD CHEM TOXICOL, V43, P581, DOI 10.1016/j.fct.2005.01.001Duty SM, 2005, HUM REPROD, V20, P604, DOI 10.1093/humrep/deh656Kota BP, 2005, PHARMACOL RES, V51, P85, DOI 10.1016/j.phrs.2004.07.012Hays T, 2005, CARCINOGENESIS, V26, P219, DOI 10.1093/carcin/bgh285Hauser R, 2004, ENVIRON HEALTH PERSP, V112, P1734, DOI 10.1289/ehp.7212Bornehag CG, 2004, ENVIRON HEALTH PERSP, V112, P1393, DOI 10.1289/ehp.7187Ishido M, 2004, J NEUROCHEM, V91, P69, DOI 10.1111/j.1471-4159.2004.02696.xMink PJ, 2004, EPIDEMIOLOGY, V15, P385, DOI 10.1097/01.ede.0000128402.86336.7eBellinger DC, 2004, EPIDEMIOLOGY, V15, P383, DOI 10.1097/01.ede.0000129525.15064.a4Shea KM, 2003, PEDIATRICS, V111, P1467Tanaka T, 2002, FOOD CHEM TOXICOL, V40, P1499, DOI 10.1016/S0278-6915(02)00073-XHoppin JA, 2002, ENVIRON HEALTH PERSP, V110, P515SATTLER JM, 2001, ASSESSMENT CHILDRENRice D, 2000, ENVIRON HEALTH PERSP, V108, P511Bellinger DC, 2000, NEUROTOXICOL TERATOL, V22, P133LIM YR, 2000, KOR J CLIN PSYCHOL, V19, P563Braissant O, 1998, ENDOCRINOLOGY, V139, P2748Peters JM, 1997, CARCINOGENESIS, V18, P2029Baldini IM, 1997, PROG NEURO-PSYCHOPH, V21, P925Roberts RA, 1997, FUND APPL TOXICOL, V38, P107PARK KS, 1996, DEV KEDI WISC INDIVIMONZANI F, 1993, CLIN INVESTIGATOR, V71, P367SILVERSTEIN AB, 1990, J CLIN PSYCHOL, V46, P333HINTON RH, 1986, ENVIRON HEALTH PERSP, V70, P195KIM MK, 1986, SEOUL J PSYCHIAT, V11, P194KAUFMAN AS, 1976, CONTEMP EDUC PSYCHOL, V1, P1801

    Insights from Amphioxus into the Evolution of Vertebrate Cartilage

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    Central to the story of vertebrate evolution is the origin of the vertebrate head, a problem difficult to approach using paleontology and comparative morphology due to a lack of unambiguous intermediate forms. Embryologically, much of the vertebrate head is derived from two ectodermal tissues, the neural crest and cranial placodes. Recent work in protochordates suggests the first chordates possessed migratory neural tube cells with some features of neural crest cells. However, it is unclear how and when these cells acquired the ability to form cellular cartilage, a cell type unique to vertebrates. It has been variously proposed that the neural crest acquired chondrogenic ability by recruiting proto-chondrogenic gene programs deployed in the neural tube, pharynx, and notochord. To test these hypotheses we examined the expression of 11 amphioxus orthologs of genes involved in neural crest chondrogenesis. Consistent with cellular cartilage as a vertebrate novelty, we find that no single amphioxus tissue co-expresses all or most of these genes. However, most are variously co-expressed in mesodermal derivatives. Our results suggest that neural crest-derived cartilage evolved by serial cooption of genes which functioned primitively in mesoderm

    Solvothermal Synthesis of Ternary Sulfides of Sb2 − xBixS3(x = 0.4, 1) with 3D Flower-Like Architectures

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    Flower-like nanostructures of Sb2 − xBixS3(x = 0.4, 1.0) were successfully prepared using both antimony diethyldithiocarbamate [Sb(DDTC)3] and bismuth diethyldithiocarbamate [Bi(DDTC)3] as precursors under solvothermal conditions at 180 °C. The prepared Sb2 − xBixS3 with flower-like 3D architectures were characterized by X-ray diffraction (XRD), scanning electron microscopy (SEM), energy dispersive X-ray spectrometry (EDS), high-resolution transmission electron microscopy (HRTEM), and selected area electron diffraction (SAED). The flower-like architectures, with an average diameter of ~4 μm, were composed of single-crystalline nanorods with orthorhombic structures. The optical absorption properties of the Sb2 − xBixS3 nanostructures were investigated by UV–Visible spectroscopy, and the results indicate that the Sb2 − xBixS3 compounds are semiconducting with direct band gaps of 1.32 and 1.30 eV for x = 0.4 and 1.0, respectively. On the basis of the experimental results, a possible growth mechanism for the flower-like Sb2 − xBixS3 nanostructures is suggested

    Modulation of RANTES expression by HCV core protein in liver derived cell lines

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    <p>Abstract</p> <p>Background</p> <p>Hepatitis C virus (HCV) infection is associated with high percentage of chronicity which implies the ability of the virus to evade or modulate host cell immune system. Modulation of chemokines, such as RANTES may be part of the virus induced pathogenicity. We examined the effect of core and structural proteins of HCV on RANTES expression in two liver derived cell lines, HepG2 and Chang Liver (CHL).</p> <p>Methods</p> <p>HepG2 and Chang Liver (CHL) cell lines were established and selected for constitutive expression of HCV core and structural genes. Flow cytometry and quantitative RT-PCR analysis were performed to examine the effect of HCV core protein on RANTES expression. Luciferase analysis after RANTES-Luc-promoter transfection of established cell lines was assayed by luminometer measurements (RLU) of RANTES promoter activity. IRF-1 and IRF-7 expression was then examined by immunoblotting analysis.</p> <p>Results</p> <p>Results of flow cytometry and RT-PCR analysis indicated that RANTES is differentially regulated by HCV core protein in the two cell lines examined as its expression was inhibited in HepG2 cells, by a reduction of RANTES promoter activity. Conversely, RANTES protein and mRNA were induced by the core protein in CHL cells, through the induction of the promoter.</p> <p>Since HCV genome modulates IRF-1 and IRF-7 in replicon system and IRF-1, IRF-3 and IRF-7 have been reported to regulate RANTES promoter in various cell systems, analysis of the mechanism underlying RANTES modulation by the core protein revealed that IRF-1 expression was induced in HepG2 cells by the core protein, whereas in CHL cells it was expressed at a very low level that was not influenced by transfection with the core protein construct. This suggested that IRF-1 level may mediate the expression of RANTES in cell lines of liver origin. The effect of the core protein on RANTES promoter was countered by co-transfection with NF90, a double-stranded-RNA binding protein that activates some interferon response genes and acts as a component of cell defense against viral infection.</p> <p>Conclusion</p> <p>HCV core protein have opposite effects on the expression of RANTES in different cell types <it>in vitro</it>, possibly reflecting a similar scenario in different microenvironments <it>in vivo</it>.</p

    Asiatic Acid Inhibits Pro-Angiogenic Effects of VEGF and Human Gliomas in Endothelial Cell Culture Models

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    Malignant gliomas are one of the most devastating and incurable tumors. Sustained excessive angiogenesis by glioma cells is the major reason for their uncontrolled growth and resistance toward conventional therapies resulting in high mortality. Therefore, targeting angiogenesis should be a logical strategy to prevent or control glioma cell growth. Earlier studies have shown that Asiatic Acid (AsA), a pentacyclic triterpenoid, is effective against glioma and other cancer cells; however, its efficacy against angiogenesis remains unknown. In the present study, we examined the anti-angiogenic efficacy of AsA using human umbilical vein endothelial cells (HUVEC) and human brain microvascular endothelial cells (HBMEC). Our results showed that AsA (5–20 µM) inhibits HUVEC growth and induces apoptotic cell death by activating caspases (3 and 9) and modulating the expression of apoptosis regulators Bad, survivin and pAkt-ser473. Further, AsA showed a dose-dependent inhibition of HUVEC migration, invasion and capillary tube formation, and disintegrated preformed capillary network. AsA also inhibited the VEGF-stimulated growth and capillary tube formation by HUVEC and HBMEC. Next, we analyzed the angiogenic potential of conditioned media collected from human glioma LN18 and U87-MG cells treated with either DMSO (control conditioned media, CCM) or AsA 20 µM (AsA20 conditioned media, AsA20CM). CCM from glioma cells significantly enhanced the capillary tube formation in both HUVEC and HBMEC, while capillary tube formation in both endothelial cell lines was greatly compromised in the presence of AsA20CM. Consistent with these results, VEGF expression was lesser in AsA20CM compared to CCM, and indeed AsA strongly inhibited VEGF level (both cellular and secreted) in glioma cells. AsA also showed dose-dependent anti-angiogenic efficacy in Matrigel plug assay, and inhibited the glioma cells potential to attract HUVEC/HBMEC. Overall, the present study clearly showed the strong anti-angiogenic potential of AsA and suggests its usefulness against malignant gliomas

    Herbal Medicines for Parkinson's Disease: A Systematic Review of Randomized Controlled Trials

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    OBJECTIVE: We conducted systematic review to evaluate current evidence of herbal medicines (HMs) for Parkinson's disease (PD). METHODS: Along with hand searches, relevant literatures were located from the electronic databases including CENTRAL, MEDLINE, EMBASE, CINAHL, AMED, PsycInfo, CNKI, 7 Korean Medical Databases and J-East until August, 2010 without language and publication status. Randomized controlled trials (RCTs), quasi-randomized controlled trials and randomized crossover trials, which evaluate HMs for idiopathic PD were selected for this review. Two independent authors extracted data from the relevant literatures and any disagreement was solved by discussion. RESULTS: From the 3432 of relevant literatures, 64 were included. We failed to suggest overall estimates of treatment effects on PD because of the wide heterogeneity of used herbal recipes and study designs in the included studies. When compared with placebo, specific effects were not observed in favor of HMs definitely. Direct comparison with conventional drugs suggested that there was no evidence of better effect for HMs. Many studies compared combination therapy with single active drugs and combination therapy showed significant improvement in PD related outcomes and decrease in the dose of anti-Parkinson's drugs with low adverse events rate. CONCLUSION: Currently, there is no conclusive evidence about the effectiveness and efficacy of HMs on PD. For establishing clinical evidence of HMs on PD, rigorous RCTs with sufficient statistical power should be promoted in future
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