49 research outputs found

    The mutations and some selected clinical findings of twenty-three carriers.

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    a<p>E: Extracellular domain; F: Furin domain; C: Collagen domain; T: TNF homology domain.</p>b<p>Hyper: hypermethylation; Hypo: hypomethylation.</p>c<p>not examined.</p>*<p>unpublished data.</p

    Relationship between methylated state and phenotype of XLHED carriers.

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    <p>Hypermethylated carriers are inclined to have more conical shaped tooth and nail dysplasia than hypomethylated group.</p

    Identification of the causative mutation in <i>EDA</i> gene.

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    <p>Arrows indicate the mutation site. The affected male patient and his mother harbored a frameshift mutation c.573–574insT.</p

    <i>EDA</i> promoter’s methylation analysis of 23 carriers.

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    <p>(A) Pyrosequencing graphs of 2 samples, a hypermethylation carrier and a hypomethylation carrier. Peak heights are proportional to the number of identical residues incorporated. Percentage in pictures means allele frequency of each site. (B) The 95% CI for the 4 sites. The figures which refer to methyl-cytosine percent at that site are calculated as described in the text. (C) The methylation state of each carriers in the 4 sites. Red, white and blue refer to hypermethylation, normal and hypomethylation respectively.</p

    Pedigree and tooth development features of the Chinese family.

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    <p>(A) Males are indicated by squares, females by circles. Affected individuals are indicated by filled symbols and unaffected individuals by white symbols. Circle containing a dot refers to carrier. An arrow indicates the proband. (B) The panoramic radiographs of the proband confirmed there was no tooth germ in the alveolar bone (red circle) which was the severest symptom of tooth dysplasia. (C) The panoramic radiographs of a healthy control with normal tooth development.</p

    Clinical phenotypes of family members in the Chinese pedigree.

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    <p>A: affected; C: carrier; F: female; M: male; NM: no missing; +: positive; number of ‘+’ symbols reflects the degree of these clinical features; -: negative; 13: Right maxillary canine; 23: Left maxillary canine.</p

    Functional analysis of genes that exhibited altered expression levels.

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    <p>Functional analysis of genes that exhibited altered expression levels.</p

    Integrated Nanoparticles To Synergistically Elevate Tumor Oxidative Stress and Suppress Antioxidative Capability for Amplified Oxidation Therapy

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    The improved antioxidant system of cancer cells renders them well-adaptive to the intrinsic oxidative stress in tumor tissues. On the other hand, cancer cells are more sensitive to elevated tumor oxidative stress as compared with normal cells due to their deficient reactive oxygen species-eliminating systems. Oxidation therapy of cancers refers to the strategy of killing cancer cells through selectively increasing the oxidative stress in tumor tissues. In this article, to amplify the oxidation therapy, we develop integrated nanoparticles with the properties to elevate tumor oxidative stress and concurrently suppress the antioxidative capability of cancer cells. The amphiphilic block copolymer micelles of poly­(ethylene glycol)-<i>b</i>-poly­[2-((((4-(4,4,5,5-tetramethyl-1,3,2-dioxaborolan-2-yl)­benzyl)­oxy)­carbonyl)­oxy)­ethyl methacrylate] (PEG-<i>b</i>-PBEMA) are integrated with palmitoyl ascorbate (PA) to form hybrid micelles (PA-Micelle). PA molecules at pharmacologic concentrations serve as a prooxidant to upregulate the hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) level in tumor sites and the PBEMA segment exhibits H<sub>2</sub>O<sub>2</sub>-triggered release of quinone methide for glutathione depletion to suppress the antioxidative capability of cancer cells, which synergistically and selectively kill cancer cells for tumor growth suppression. Given the significantly low side toxicity against normal tissues, this novel integrated nanoparticle design represents a novel class of nanomedicine systems for high-efficiency oxidation therapy with the potentials to be translated to clinical applications
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