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991.
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Emma Jane Poulton Lisa Levy Johanna W. Lampe Danny D. Shen Julia Tracy Margaret C. Shuhart Kenneth E. Thummel David L. Eaton 《Toxicology and applied pharmacology》2013,266(1):122-131
Sulforaphane (SFN), is an effective in vitro antagonist of ligand activation of the human pregnane and xenobiotic receptor (PXR). PXR mediated CYP3A4 up-regulation is implicated in adverse drug-drug interactions making identification of small molecule antagonists a desirable therapeutic goal. SFN is not an antagonist to mouse or rat PXR in vitro; thus, normal rodent species are not suitable as in vivo models for human response. To evaluate whether SFN can effectively antagonize ligand activation of human PXR in vivo, a three-armed, randomized, crossover trial was conducted with 24 healthy adults. The potent PXR ligand — rifampicin (300 mg/d) was given alone for 7 days in arm 1, or in daily combination with 450 μmol SFN (Broccoli Sprout extract) in arm 2; SFN was given alone in arm 3. Midazolam as an in vivo phenotype marker of CYP3A was administered before and after each treatment arm. Rifampicin alone decreased midazolam AUC by 70%, indicative of the expected increase in CYP3A4 activity. Co-treatment with SFN did not reduce CYP3A4 induction. Treatment with SFN alone also did not affect CYP3A4 activity in the cohort as a whole, although in the subset with the highest basal CYP3A4 activity there was a statistically significant increase in midazolam AUC (i.e., decrease in CYP3A4 activity). A parallel study in humanized PXR mice yielded similar results. The parallel effects of SFN between humanized PXR mice and human subjects demonstrate the predictive value of humanized mouse models in situations where species differences in ligand-receptor interactions preclude the use of a native mouse model for studying human ligand-receptor pharmacology. 相似文献
994.
Marian N. Zappala Joanne T. Ellzey Julia Bader Jose R. Peralta-Videa Jorge Gardea-Torresdey 《Archives of environmental contamination and toxicology》2013,65(2):212-223
Due to health reasons, toxic metals must be removed from soils contaminated by mine tailings and smelter activities. The phytoremediation potential of Prosopis pubescens (screw bean mesquite) was examined by use of inductively-coupled plasma optical emission spectroscopy. Transmission electron microscopy was used to observe ultrastructural changes of parenchymal cells of leaves in the presence of copper. Elemental analysis was used to localize copper within leaves. A 600-ppm copper sulfate exposure to seedlings for 24 days resulted in 31,000 ppm copper in roots, 17,000 ppm in stems, 11,000 in cotyledons and 20 ppm in the true leaves. For a plant to be considered a hyperaccumulator, the plant must accumulate a leaf-to-root ratio <1. Screw bean mesquite exposed to copper had a leaf-to-root ratio of 0.355 when cotyledons were included. We showed that P. pubescens grown in soil is a hyperaccumulator of copper. We recommend that this plant should be field tested. 相似文献
995.
Growth curves of “normal” serum total IgE levels throughout childhood: A quantile analysis in a birth cohort 下载免费PDF全文
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997.
Iryna Ziabreva Graham Campbell Julia Rist Jessica Zambonin Joanna Rorbach Mateusz M. Wydro Hans Lassmann Robin J. M. Franklin Don Mahad 《Glia》2010,58(15):1827-1837
Oligodendrocyte lineage cells are susceptible to a variety of insults including hypoxia, excitotoxicity, and reactive oxygen species. Demyelination is a well‐recognized feature of several CNS disorders including multiple sclerosis, white matter strokes, progressive multifocal leukoencephalopathy, and disorders due to mitochondrial DNA mutations. Although mitochondria have been implicated in the demise of oligodendrocyte lineage cells, the consequences of mitochondrial respiratory chain defects have not been examined. We determine the in vitro impact of established inhibitors of mitochondrial respiratory chain complex IV or cytochrome c oxidase on oligodendrocyte progenitor cells (OPCs) and mature oligodendrocytes as well as on differentiation capacity of OPCs from P0 rat. Injury to mature oligodendrocytes following complex IV inhibition was significantly greater than to OPCs, judged by cell detachment and mitochondrial membrane potential (MMP) changes, although viability of cells that remained attached was not compromised. Active mitochondria were abundant in processes of differentiated oligodendrocytes and MMP was significantly greater in differentiated oligodendrocytes than OPCs. MMP dissipated following complex IV inhibition in oligodendrocytes. Furthermore, complex IV inhibition impaired process formation within oligodendrocyte lineage cells. Injury to and impaired process formation of oligodendrocytes following complex IV inhibition has potentially important implications for the pathogenesis and repair of CNS myelin disorders. © 2010 Wiley‐Liss, Inc. 相似文献
998.
Julia S. Lehman MD Shahrukh K. Hashmi MD MPH Hillard M. Lazarus MD Rokea A. el‐Azhary MD PhD Lawrence E. Gibson MD William J. Hogan MD Mark R. Litzow MD Mrinal S. Patnaik MBBS Francis Buadi MD Martha Q. Lacy MD Surendra Dasari PhD Patrick Vanderboom MS Alexander Meves MD PhD 《Journal of cutaneous pathology》2017,44(12):1087-1091
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Judith Espinosa-Raya Sofía Díaz-Cintra Julia Segura-Uribe Sandra Orozco-Suárez Juan Manuel Gallardo Christian Guerra-Araiza 《中国神经再生研究》2017,(4):588-595
Aging is a key risk factor for cognitive decline and age-related neurodegenerative disorders. Also, an age-related decrease in sex steroid hormones may have a negative impact on the formation of neurofibrillary tangles(NFTs); these hormones can regulate Tau phosphorylation and the principal kinase GSK3β involved in this process. Hormone replacement therapy decreases NFTs, but it increases the risk of some types of cancer. However, other synthetic hormones such as tibolone(TIB) have been used for hormone replacement therapy. The aim of this work was to evaluate the long-term effects of TIB(0.01 mg/kg and 1 mg/kg, intragastrically for 12 weeks) on the content of total and hyperphosphorylated Tau(PHF-1) proteins and the regulation of GSK3β/Akt/PI3 K pathway and CDK5/p35/p25 complexes in the hippocampus of aged male mice. We observed that the content of PHF-1 decreased with TIB administration. In contrast, no changes were observed in the active form of GSK3β or PI3 K. TIB decreased the expression of the total and phosphorylated form of Akt while increased that of p110 and p85. The content of CDK5 was differentially modified with TIB: it was increased at low doses and decreased at high doses. When we analyzed the content of CDK5 activators, an increase was found on p35; however, the content of p25 decreased with administration of low dose of TIB. Our results suggest a possible mechanism of action of TIB in the hippocampus of aged male mice. Through the regulation of Tau and GSK3β/Akt/PI3 K pathway, and CDK5/p35/p25 complexes, TIB may modulate neuronal plasticity and regulate learning and memory processes. 相似文献