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              <text>&lt;a href="http://doi.org/10.2174/187152412800792670" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.2174/187152412800792670&lt;/a&gt;</text>
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              <text>95–99</text>
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              <text>2</text>
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                <text>The blood-brain barrier choline transporter.</text>
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                <text>Central nervous system agents in medicinal chemistry</text>
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                <text>Humans; Animals; Drug Delivery Systems/*methods; Blood-Brain Barrier/drug effects/*metabolism; Membrane Transport Proteins/*metabolism; Organic Cation Transport Proteins/metabolism; Organic Cation Transporter 1/metabolism; Organic Cation Transporter 2</text>
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                <text>Geldenhuys Werner J; Allen David D</text>
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                <text>Drug delivery to the brain is made difficult by the blood-brain barrier (BBB) which is selectively permeable to organic drug compounds. Several membrane solute and nutrient transporters are expressed in the BBB vasculature, which may be utilized as mechanism of delivery of drugs to the brain. Of interest to us, are the organic cation transporters which could be used to transport cationic compounds into the CNS. In this mini-review, we will review the current understanding of the structural requirements for designing compounds which could effectively use organic cation transporters (OCT). For the first time, structural requirements for both OCT1 and OCT2 versus the BBB choline transporter (BBBCHT) are discussed and compared. The information gained here could increase the success rate in successful CNS drug delivery and therapeutics.</text>
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              <text>&lt;a href="http://doi.org/10.1111/nyas.13156" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1111/nyas.13156&lt;/a&gt;</text>
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              <text>80–86</text>
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              <text>1</text>
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                <text>Novel approaches to mitigating parathion toxicity: targeting cytochrome</text>
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                <text>*menadione; *organophosphorus pesticides; *paraoxon; *parathion; *redox cycling; Animals; Cholinesterase Inhibitors/metabolism/*toxicity; Cytochrome P-450 Enzyme Inhibitors/*administration &amp; dosage/metabolism; Cytochrome P-450 Enzyme System/metabolism; Drug Delivery Systems/*methods; Humans; Insecticides/metabolism/toxicity; Organophosphate Poisoning/drug therapy/enzymology; Parathion/metabolism/*toxicity; Vitamin K 3/*administration &amp; dosage/metabolism</text>
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                <text>Jan Yi-Hua; Richardson Jason R; Baker Angela A; Mishin Vladimir; Heck Diane E; Laskin Debra L; Laskin Jeffrey D</text>
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                <text>Accidental or intentional exposures to parathion, an organophosphorus (OP) pesticide, can cause severe poisoning in humans. Parathion toxicity is dependent on its metabolism by the cytochrome P450 (CYP) system to paraoxon (diethyl</text>
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                <text>&lt;a href="http://doi.org/10.1111/nyas.13156" target="_blank" rel="noreferrer noopener"&gt;10.1111/nyas.13156&lt;/a&gt;</text>
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              <text>10</text>
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              <text>44</text>
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                <text>Preparation of emulsifying wax/glyceryl monooleate nanoparticles and evaluation as a delivery system for repurposing simvastatin in bone regeneration.</text>
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                <text>Animals; bone; Bone Regeneration/*drug effects/physiology; drug delivery; Drug Delivery Systems/*methods; Drug Evaluation; Drug Repositioning/methods; Emulsifying Agents/administration &amp; dosage/*chemical synthesis; Glycerides/administration &amp; dosage/*chemical synthesis; Mice; nanoemulsions; nanoparticles; Nanoparticles/administration &amp; dosage/*chemistry; osteoblasts; Osteoblasts/drug effects/physiology; Osteoclasts; Preclinical/methods; RAW 264.7 Cells; Simvastatin/administration &amp; dosage/*chemical synthesis; Waxes/chemical synthesis/pharmacology</text>
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                <text>Eskinazi-Budge Aaron; Manickavasagam Dharani; Czech Tori; Novak Kimberly; Kunzler James; Oyewumi Moses O</text>
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                <text>Simvastatin (Sim) is a widely known drug in the treatment of hyperlipidemia, which has attracted so much attention in bone regeneration due to its potential osteoanabolic effect. However, repurposing of Sim in bone regeneration will require suitable delivery systems that can negate undesirable off-target/side effects. In this study, we have investigated a new lipid nanoparticle (NP) platform that was fabricated using a binary blend of emulsifying wax (Ewax) and glyceryl monooleate (GMO). Using the binary matrix materials, NPs loaded with Sim (0-500 microg/mL) were prepared and showed an average particle size of about 150 nm. NP size stability was dependent on Sim concentration loaded in NPs. The suitability of NPs prepared with the binary matrix materials in Sim delivery for potential application in bone regeneration was supported by biocompatibility in pre-osteoclastic and pre-osteoblastic cells. Additional data demonstrated that biofunctional Sim was released from NPs that facilitated differentiation of osteoblasts (cells that form bones) while inhibiting differentiation of osteoclasts (cells that resorb bones). The overall work demonstrated the preparation of NPs from Ewax/GMO blends and characterization to ascertain potential suitability in Sim delivery for bone regeneration. Additional studies on osteoblast and osteoclast functions are warranted to fully evaluate the efficacy of Sim-loaded Ewax/GMO NPs using in-vitro and in-vivo approaches.</text>
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              <elementText elementTextId="51007">
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        <name>Oyewumi Moses O</name>
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              <text>&lt;a href="http://doi.org/10.1016/j.ejpb.2014.07.011" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/j.ejpb.2014.07.011&lt;/a&gt;</text>
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              <text>962–972</text>
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              <text>88</text>
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                <text>Formulation and photoirradiation parameters that influenced photoresponsive drug delivery using alkoxylphenacyl-based polycarbonates.</text>
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                <text>European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V</text>
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                <text>2014-11</text>
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              <elementText elementTextId="44074">
                <text>Animals; Biocompatibility; Cardiotoxicity; Cell Line; Chemistry; Dose-Response Relationship; Doxorubicin; Drug; Drug Delivery Systems/*methods; Heart/drug effects; Humans; Inbred BALB C; Mice; Nanotechnology; Pharmaceutical; Photic Stimulation/*methods; Photoresponsive; Photosensitizing Agents/*chemical synthesis/radiation effects/toxicity; Polycarboxylate Cement/*chemical synthesis/radiation effects/toxicity; Polymer chain scission; Stimuli-responsive; Tumor</text>
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              <elementText elementTextId="44075">
                <text>Wehrung Daniel; Chamsaz Elaheh A; Joy Abraham; Oyewumi Moses O</text>
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          <element elementId="41">
            <name>Description</name>
            <description>An account of the resource</description>
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                <text>Recently, we reported the synthesis and biocompatibility of alkoxylphenacyl-based polycarbonates (APP); a promising new class of polymers that undergo photo-induced chain scission. In the current study, nanoparticles (NPs) were prepared from the APP polymer (APP-NPs) and loaded with doxorubicin (DOX) (DOX-APP-NPs) in order to identify and evaluate formulation and photoirradiation parameters that influence photoresponsive efficacy. Stable and spherical APP-NPs were prepared with diameters between 70-80nm depending on APP concentration (10-40mg/mL). There was a direct relationship between APP concentration and resultant particle size. Drug release studies indicated that exposure to the photo-trigger was capable of altering the rate and extent of DOX released. Photoresponsive DOX release was markedly influenced by the frequency of photoirradiation while the effect of APP concentration was most likely propagated through NP size. DOX released by photoactivation retained its efficacy as assessed by cytotoxicity studies in human lung adenocarcinoma (A549) cells. Studies in BALB/c mice indicated that DOX-APP-NPs induce less cardiotoxicity than DOX alone and that DOX-APP-NPs are not susceptible to dose dumping after photoirradiation.</text>
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                <text>&lt;a href="http://doi.org/10.1016/j.ejpb.2014.07.011" target="_blank" rel="noreferrer noopener"&gt;10.1016/j.ejpb.2014.07.011&lt;/a&gt;</text>
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              <elementText elementTextId="44079">
                <text>Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).</text>
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        <name>Chamsaz Elaheh A</name>
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        <name>Department of Pharmaceutical Sciences</name>
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        <name>European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V</name>
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        <name>Photoresponsive</name>
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        <name>Photosensitizing Agents/*chemical synthesis/radiation effects/toxicity</name>
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        <name>Polycarboxylate Cement/*chemical synthesis/radiation effects/toxicity</name>
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        <name>Polymer chain scission</name>
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        <name>Stimuli-responsive</name>
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            <elementText elementTextId="43267">
              <text>&lt;a href="http://doi.org/10.1016/j.bmcl.2009.12.088" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/j.bmcl.2009.12.088&lt;/a&gt;</text>
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              <text>819–823</text>
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          <elementTextContainer>
            <elementText elementTextId="43270">
              <text>3</text>
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            <elementText elementTextId="43271">
              <text>20</text>
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                <text>Structure-based design of a thiazolidinedione which targets the mitochondrial protein mitoNEET.</text>
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            <name>Publisher</name>
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                <text>Bioorganic &amp; medicinal chemistry letters</text>
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                <text>2010</text>
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              <elementText elementTextId="43262">
                <text>2010-02</text>
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                <text>*Drug Design; Animals; Binding Sites/drug effects/physiology; Dose-Response Relationship; Drug; Drug Delivery Systems/*methods; Liver/drug effects/metabolism; Mitochondria; Mitochondrial Proteins/*metabolism; Protein Structure; Rats; Secondary; Structure-Activity Relationship; Thiazolidinediones/administration &amp; dosage/*chemical synthesis/*metabolism</text>
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                <text>Geldenhuys Werner J; Funk Max O; Barnes Kendra F; Carroll Richard T</text>
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                <text>Several PPAR-gamma agonists containing a thiazolidinedione moiety (referred to as glitazones) have been proposed to be neuroprotective and appear to alter mitochondrial function. Recently, a search for mitochondrial proteins that bind pioglitazone identified a novel protein, mitoNEET, which was later shown to regulate the oxidative capacity of the mitochondria. This identified an alternative target for the glitazones suggesting a possible new drug target for the treatment of neurodegenerative diseases. Molecular docking studies employing the reported crystal structure revealed five possible binding pockets on mitoNEET. We focused on two sites based on their physical characteristics. Using binding information gained from the analysis of two glitazones docked in these pockets, we designed and synthesized a ligand (NL-1) that would preferentially bind to site 1. Based on [(3)H]-binding data of the glitazones and comparisons to computer generated K(i)s, we were able to predict that site 1 was likely the target of the glitazones. NL-1 uncoupled isolated mitochondrial complex I respiration with an IC(50) of 2.4 microM and inhibited state III respiration up to 45%. To investigate the ability of NL-1 to block rotenone initiated free radicals from complex I, we found it was able to protect the human neuronal cell line SH-SY5Y against rotenone induced cell death. These data demonstrate that mitoNEET is a viable target for the design and synthesis of novel therapeutic agents aimed at altering mitochondrial function.</text>
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            <name>Identifier</name>
            <description>An unambiguous reference to the resource within a given context</description>
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                <text>&lt;a href="http://doi.org/10.1016/j.bmcl.2009.12.088" target="_blank" rel="noreferrer noopener"&gt;10.1016/j.bmcl.2009.12.088&lt;/a&gt;</text>
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            <name>Rights</name>
            <description>Information about rights held in and over the resource</description>
            <elementTextContainer>
              <elementText elementTextId="43268">
                <text>Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).</text>
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        <name>Thiazolidinediones/administration &amp; dosage/*chemical synthesis/*metabolism</name>
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