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<script type="text/javascript" src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/jr.boots.min.js"> </script><title>Anti-ICAM-1 antibody-conjugated paramagnetic liposomes - Molecular Imaging and Contrast Agent Database (MICAD) - NCBI Bookshelf</title>
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<meta name="citation_inbook_title" content="Molecular Imaging and Contrast Agent Database (MICAD) [Internet]">
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<meta name="citation_title" content="Anti-ICAM-1 antibody-conjugated paramagnetic liposomes">
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<meta name="citation_date" content="2008/02/14">
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<meta name="citation_author" content="Huiming Zhang">
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<meta name="citation_pmid" content="20641750">
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<meta name="DC.Title" content="Anti-ICAM-1 antibody-conjugated paramagnetic liposomes">
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<meta name="DC.Contributor" content="Huiming Zhang">
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<meta name="description" content="ICAM-1 (CD54) is a cell-surface glycoprotein belonging to the immunoglobulin superfamily of cell adhesion molecules (CAMs) (1). Upregulated by inflammatory mediators, ICAM-1 is expressed on various cells including leukocytes, epithelial cells, endothelial cells, and fibroblasts (2). The predominant function of ICAM-1 is the recruitment and trafficking of leukocytes through interactions with leukocyte-expressed integrins (2). Therefore, ICAM-1 plays a critical role in the development of the central nervous system (CNS), in immune and inflammatory responses, and in embryonic development (1). Many cerebrovascular and neurological diseases such as multiple sclerosis and its animal model (i.e., experimental allergic encephalomyelitis (EAE)), Alzheimer’s disease, and Parkinson’s disease have neuroinflammatory responses involving the migration of leukocytes into damaged or infected tissues (3). EAE, which is an ascending encephalomyelitis, is characterized by an intense perivascular inflammatory process in the white matter of the CNS, primarily on the spinal cord, brainstem, and cerebellum, which facilitates the attachment of leukocytes to inflamed endothelium (4). For example, a 10-fold increase in ICAM-1 expression has been found on the endothelium of capillaries and venules throughout the CNS at an early stage of EAE (4). Thus, ICAM-1 has been an attractive target for imaging the early and specific upregulation of vascular CAMs in diseases (4).">
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<meta name="og:description" content="ICAM-1 (CD54) is a cell-surface glycoprotein belonging to the immunoglobulin superfamily of cell adhesion molecules (CAMs) (1). Upregulated by inflammatory mediators, ICAM-1 is expressed on various cells including leukocytes, epithelial cells, endothelial cells, and fibroblasts (2). The predominant function of ICAM-1 is the recruitment and trafficking of leukocytes through interactions with leukocyte-expressed integrins (2). Therefore, ICAM-1 plays a critical role in the development of the central nervous system (CNS), in immune and inflammatory responses, and in embryonic development (1). Many cerebrovascular and neurological diseases such as multiple sclerosis and its animal model (i.e., experimental allergic encephalomyelitis (EAE)), Alzheimer’s disease, and Parkinson’s disease have neuroinflammatory responses involving the migration of leukocytes into damaged or infected tissues (3). EAE, which is an ascending encephalomyelitis, is characterized by an intense perivascular inflammatory process in the white matter of the CNS, primarily on the spinal cord, brainstem, and cerebellum, which facilitates the attachment of leukocytes to inflamed endothelium (4). For example, a 10-fold increase in ICAM-1 expression has been found on the endothelium of capillaries and venules throughout the CNS at an early stage of EAE (4). Thus, ICAM-1 has been an attractive target for imaging the early and specific upregulation of vascular CAMs in diseases (4).">
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id="jr-fip-info-p"><a id="jr-fip-prev" class="wsprkl btn" title="Jump to previuos match">◀</a><button id="jr-fip-matches">no matches yet</button><a id="jr-fip-next" class="wsprkl btn" title="Jump to next match">▶</a></nav></nav></div><div id="jr-epub-interstitial" class="hidden"></div><div id="jr-content"><article data-type="main"><div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><div class="fm-sec"><h1 id="_NBK23552_"><span class="title" itemprop="name">Anti-ICAM-1 antibody-conjugated paramagnetic liposomes</span></h1><div itemprop="alternativeHeadline" class="subtitle whole_rhythm">Anti-ICAM ACPLs</div><p class="contribs">Zhang H.</p><p class="fm-aai"><a href="#_NBK23552_pubdet_">Publication Details</a></p></div></div><div class="jig-ncbiinpagenav body-content whole_rhythm" data-jigconfig="allHeadingLevels: ['h2'],smoothScroll: false" itemprop="text"><div class="iconblock whole_rhythm clearfix ten_col table-wrap" id="figICAMACPLsT1"><a href="/books/NBK23552/table/ICAM_ACPLs.T1/?report=objectonly" target="object" title="Table" class="img_link icnblk_img" rid-ob="figobICAMACPLsT1"><img class="small-thumb" src="/corehtml/pmc/css/bookshelf/2.26/img/table-icon.gif" alt="Table Icon" /></a><div class="icnblk_cntnt"><h4 id="ICAM_ACPLs.T1"><a href="/books/NBK23552/table/ICAM_ACPLs.T1/?report=objectonly" target="object" rid-ob="figobICAMACPLsT1">Table</a></h4><p class="float-caption no_bottom_margin">
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<i>In vitro</i>
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Rodents
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</p></div></div><div id="ICAM_ACPLs.Background"><h2 id="_ICAM_ACPLs_Background_">Background</h2><p>[<a href="/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=paramagnetic%20liposome%20ICAM" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>ICAM-1 (CD54) is a cell-surface glycoprotein belonging to the immunoglobulin superfamily of cell adhesion molecules (CAMs) (<a class="bibr" href="#ICAM_ACPLs.REF.1" rid="ICAM_ACPLs.REF.1">1</a>). Upregulated by inflammatory mediators, ICAM-1 is expressed on various cells including leukocytes, epithelial cells, endothelial cells, and fibroblasts (<a class="bibr" href="#ICAM_ACPLs.REF.2" rid="ICAM_ACPLs.REF.2">2</a>). The predominant function of ICAM-1 is the recruitment and trafficking of leukocytes through interactions with leukocyte-expressed integrins (<a class="bibr" href="#ICAM_ACPLs.REF.2" rid="ICAM_ACPLs.REF.2">2</a>). Therefore, ICAM-1 plays a critical role in the development of the central nervous system (CNS), in immune and inflammatory responses, and in embryonic development (<a class="bibr" href="#ICAM_ACPLs.REF.1" rid="ICAM_ACPLs.REF.1">1</a>). Many cerebrovascular and neurological diseases such as multiple sclerosis and its animal model (i.e., experimental allergic encephalomyelitis (EAE)), Alzheimer’s disease, and Parkinson’s disease have neuroinflammatory responses involving the migration of leukocytes into damaged or infected tissues (<a class="bibr" href="#ICAM_ACPLs.REF.3" rid="ICAM_ACPLs.REF.3">3</a>). EAE, which is an ascending encephalomyelitis, is characterized by an intense perivascular inflammatory process in the white matter of the CNS, primarily on the spinal cord, brainstem, and cerebellum, which facilitates the attachment of leukocytes to inflamed endothelium (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>). For example, a 10-fold increase in ICAM-1 expression has been found on the endothelium of capillaries and venules throughout the CNS at an early stage of EAE (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>). Thus, ICAM-1 has been an attractive target for imaging the early and specific upregulation of vascular CAMs in diseases (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>).</p><p>Amphiphiles are made from molecules containing both a hydrophobic (non-polar tail) and a hydrophilic (polar head) section. Amphiphiles can self-associate into multiple concentric lipid bilayers (called lamellae) in different sizes and geometries (<a class="bibr" href="#ICAM_ACPLs.REF.5" rid="ICAM_ACPLs.REF.5">5</a>). Liposomes are generally formed by a variety of modified amphiphiles and can deliver a substantial amount of encapsulated therapeutic or diagnostic agents to targeted sites (<a class="bibr" href="#ICAM_ACPLs.REF.6" rid="ICAM_ACPLs.REF.6">6</a>). Traditional liposomes suffer from the drawbacks of fast elimination from blood and easy capture by the reticulo-endothelial system (<a class="bibr" href="#ICAM_ACPLs.REF.7" rid="ICAM_ACPLs.REF.7">7</a>). As an alternative to traditional liposomes, paramagnetic polymerized liposomes (PPLs) are composed of a mixture of lipids with different functional groups on the aqueous exposed surface and a polymerizable group (diacetylene) in the lipid tail (<a class="bibr" href="#ICAM_ACPLs.REF.8" rid="ICAM_ACPLs.REF.8">8</a>). A typical formulation consists of gadolinium III–diethylenetriamine pentaacetic acid (Gd-DTPA)–based lipids, amphiphilic carrier lipids, and biotinylated amphiphiles (<a class="bibr" href="#ICAM_ACPLs.REF.9" rid="ICAM_ACPLs.REF.9">9</a>).</p><p>PPLs possess increased physical stability, unique spectroscopic properties, and chemical modification durability (<a class="bibr" href="#ICAM_ACPLs.REF.9" rid="ICAM_ACPLs.REF.9">9</a>). The diacetylene triple bonds in the PPLs are located in the fatty acyl chains. The polymerization of the triple bonds between lipids can be carried out by simple ultraviolet (UV) radiation to form a polydiacetylene backbone of alternating eneyne groups (<a class="bibr" href="#ICAM_ACPLs.REF.8" rid="ICAM_ACPLs.REF.8">8</a>). A short polyethylene glycol (PEG) segment is covalently linked to the polar head of PPLs (<a class="bibr" href="#ICAM_ACPLs.REF.9" rid="ICAM_ACPLs.REF.9">9</a>). The hydrophilicity of PEG allows for sterical stabilization of PPLs and protects against interactions with other molecular and biological components in blood stream, such as undesired lipid exchange or lipid fusion (<a class="bibr" href="#ICAM_ACPLs.REF.9" rid="ICAM_ACPLs.REF.9">9</a>). Both polymerization and PEGylization prolong the <i>in vivo</i> circulation time of PPLs in blood. For instance, the half-life time of the PPLs is found to be ~19 h in rats (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>). Because easy access to bulky water, the attachment of Gd-DTPA chelates on the surface of PPLs allows for greater relaxivity enhancement compared to Gd chelates entrapped in the traditional liposomes. The multiple Gd chelates on the surface of the liposomes further increase the sensitivity to detection by magnetic resonance imaging (MRI). The biotin groups in the PPLs allow for conjugation of biotinylated antibodies <i>via</i> an avidin-biotin linkage procedure (<a class="bibr" href="#ICAM_ACPLs.REF.10" rid="ICAM_ACPLs.REF.10">10</a>). Avidin, a tetrameric protein with a molecular mass of 68 KDa, is capable of strongly binding four biotins (K<sub>a</sub> = 1.7 × 10<sup>15</sup> M<sup>-1</sup>) (<a class="bibr" href="#ICAM_ACPLs.REF.10" rid="ICAM_ACPLs.REF.10">10</a>). Thus, avidins serve as a bridge between a biotinylated antibody against neural CAM (NCAM-1) and a biotinylated group on PPLs to form a NCAM-1–specific MRI contrast agent, anti-NCAM antibody-conjugated PPLs (ACPLs) (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>).</p></div><div id="ICAM_ACPLs.Synthesis"><h2 id="_ICAM_ACPLs_Synthesis_">Synthesis</h2><p>[<a href="/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=(paramagnetic%20liposome%20ICAM)+AND+synthesis%0D%0A" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>Storrs et al. reported the details of synthesis of PPLs (<a class="bibr" href="#ICAM_ACPLs.REF.9" rid="ICAM_ACPLs.REF.9">9</a>). Pentacosadiynoic acid (PDA) was treated with N-hydroxysuccinimide (NHS) and 1-(3-(dimethylamino)propyl)-3-ethylcarbodiimide hydrochloride (EDC) to form NHS ester, which was treated with a PEG-diamine linker (NH<sub>2</sub>(CH<sub>2</sub>CH<sub>2</sub>O)<sub>2</sub>CH<sub>2</sub>CH<sub>2</sub>NH<sub>2</sub>) to produce PEG-PDA derivatives. Then, the product was treated with DTPA dianhydride (DTPAA) to form DTPA-bis(PEG-PDA) diamides followed by a complexation with GdCl<sub>3</sub> to produce a neutral amphiphilic Gd chelates. The PEG-PDA derivative was treated with biotinamidocaproic acid NHS ester to form biotinylated lipid conjugates. To generate PPLs, a mixture of 60% PEG-PDA, 29.5% Gd chelate lipid , 10% amino-terminated lipid, and 0.5% biotinylated lipid was polymerized at 0°C under irradiation from an ultraviolet lamp (wavelength = 254 nm) to form a dark blue PDA-PPLs. Sipkins et al. reported the details of preparation of anti–NCAM-1 ACPLs from the PPLs (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>). ACPLs were formed by the addition of 2.3 μg avidin and 14.9 μg biotinylated antibody in a PPL solution at a concentration of 5.6 mM acyl chains.</p></div><div id="ICAM_ACPLs.In_Vitro_Studies_Tes"><h2 id="_ICAM_ACPLs_In_Vitro_Studies_Tes_"><i>In Vitro</i> Studies: Testing in Cells and Tissues</h2><p>[<a href="/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=(%20paramagnetic%20liposome%20ICAM)+AND+%22in+vitro%22" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>The T<sub>1</sub> relaxivity of PPLs was determined to be 8.7 mM<sup>-1</sup>•s<sup>-1</sup> at 2.0 T (<a class="bibr" href="#ICAM_ACPLs.REF.8" rid="ICAM_ACPLs.REF.8">8</a>, <a class="bibr" href="#ICAM_ACPLs.REF.9" rid="ICAM_ACPLs.REF.9">9</a>). Gel electrophoresis and immunodetection techniques demonstrated the capability of attaching the monoclonal antibodies to biotinylated PPLs. The binding specificity of anti-ICAM-1 ACPLs was examined with an enzyme-linked immunosorbent assay (ELISA) in which the anti–ICAM-1 ACPLs competed with the inhibitory binding of horseradish peroxidase (HRP)-labeled anti–ICAM-1 antibodies (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>). Then, the anti–ICAM-1 ACPL recognition of antigens was further confirmed in cultured endothelial cells with bacterial lipopolysaccharide–stimulated ICAM-1 expression. The multivalent anti–ICAM-1 ACPLs appeared to have significantly higher binding affinities compared to free antibody.</p></div><div id="ICAM_ACPLs.Animal_Studies"><h2 id="_ICAM_ACPLs_Animal_Studies_">Animal Studies</h2><div id="ICAM_ACPLs.Rodents"><h3>Rodents</h3><p>[<a href="/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=(%20paramagnetic%20liposome%20ICAM)%20+AND++rodentia" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>The <i>in vivo</i> targeting of anti–ICAM-1 ACPLs was examined in mice with EAE (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>). Texas Red fluorophore-labeled anti-NCAM-1 ACPLs were administrated intravenously to EAE mice at 1.2 mg Gd/kg and 890 μg antibody/kg in the early phase of ICAM-1 upregulation. At 24 h after injection, brains were harvested for microscopic localization of fluorescent ACPLs. All EAE mice showed positive ACPL binding to CNS microvasculature in the cerebellum, brainstem, and spinal cord (<a class="bibr" href="#ICAM_ACPLs.REF.4" rid="ICAM_ACPLs.REF.4">4</a>). The location of anti–ICAM-1 binding appeared to correlate with the immunohistochemically defined patterns for ICAM-1 expressions. For example, the binding of anti–ICAM-1 ACPLs was found in multiple vessels in the cerebellum that were surrounded by inflammatory infiltrates, in microvessels that were not associated with inflammatory infiltrates, and in small vessels but not in the large central arterioles. The complementary halves of the mouse brains were reserved from the fluorescence microscopy experiments and further imaged with high-resolution MRI microscopy techniques. Each brain was fixed in 45% paraformaldehyde, and T<sub>1</sub>-weighted images were collected on a 9.4 T imager. There were substantial increases in MRI signal intensity in the cerebellar (32%) and cerebral (28%) cortex, with moderate signal intensity increases in the cerebellar white matter (18%). The contrast between gray and white matter was improved particularly in the cerebellum because gray matter was significantly more vascularized than white matter. The PPLs had a blood plasma half-life of 19 h, which was comparable to that of PEG-stabilized liposomes (<a class="bibr" href="#ICAM_ACPLs.REF.9" rid="ICAM_ACPLs.REF.9">9</a>).</p></div><div id="ICAM_ACPLs.Other_NonPrimate_Mam"><h3>Other Non-Primate Mammals</h3><p>[<a href="/entrez/query.fcgi?cmd=PureSearch&db=pubmed&details_term=%22%20SUBSTANCENAME%22%5BSubstance%20Name%5D%20AND%20%28dog%20OR%20rabbit%20OR%20pig%20OR%20sheep%29" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>No publication is currently available.</p></div><div id="ICAM_ACPLs.NonHuman_Primates"><h3>Non-Human Primates</h3><p>[<a href="/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=(%20paramagnetic%20liposome%20ICAM)%20+AND+(primate+non+human)" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>No publication is currently available.</p></div></div><div id="ICAM_ACPLs.Human_Studies"><h2 id="_ICAM_ACPLs_Human_Studies_">Human Studies</h2><p>[<a href="/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=(%20paramagnetic%20liposome%20ICAM)%20+AND+human" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>No publication is currently available.</p><div id="ICAM_ACPLs.NIH_Support"><h3>NIH Support</h3><p>GM 07365</p></div></div><div id="ICAM_ACPLs.references"><h2 id="_ICAM_ACPLs_references_">References</h2><dl class="temp-labeled-list"><dl class="bkr_refwrap"><dt>1.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.1">Hubbard A.K. , Rothlein R. Intercellular adhesion molecule-1 (ICAM-1) expression and cell signaling cascades. <span><span class="ref-journal">Free Radic Biol Med. </span>2000;<span class="ref-vol">
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<strong>28</strong>
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</span>(9):1379–86.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/10924857" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 10924857</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>2.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.2">Hopkins A.M. , Baird A.W. , Nusrat A. ICAM-1: targeted docking for exogenous as well as endogenous ligands. <span><span class="ref-journal">Adv Drug Deliv Rev. </span>2004;<span class="ref-vol">
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<strong>56</strong>
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</span>(6):763–78.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/15063588" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15063588</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>3.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.3">Turowski P. , Adamson P. , Greenwood J. Pharmacological targeting of ICAM-1 signaling in brain endothelial cells: potential for treating neuroinflammation. <span><span class="ref-journal">Cell Mol Neurobiol. </span>2005;<span class="ref-vol">
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<strong>25</strong>
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</span>(1):153–70.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/15962512" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15962512</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>4.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.4">Sipkins D.A. , Gijbels K. , Tropper F.D. , Bednarski M. , Li K.C. , Steinman L. ICAM-1 expression in autoimmune encephalitis visualized using magnetic resonance imaging. <span><span class="ref-journal">J Neuroimmunol. </span>2000;<span class="ref-vol">
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</span>(1):1–9.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/10683508" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 10683508</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>5.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.5">Baxter A.G. The origin and application of experimental autoimmune encephalomyelitis. <span><span class="ref-journal">Nat Rev Immunol. </span>2007;<span class="ref-vol">
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<strong>7</strong>
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</span>(11):904–12.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/17917672" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 17917672</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>6.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.6">Strijkers G.J. , Mulder W.J. , van Heeswijk R.B. , Frederik P.M. , Bomans P. , Magusin P.C. , Nicolay K. Relaxivity of liposomal paramagnetic MRI contrast agents. <span><span class="ref-journal">Magma. </span>2005;<span class="ref-vol">
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<strong>18</strong>
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</span>(4):186–92.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/16155762" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 16155762</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>7.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.7">Torchilin V.P. Recent advances with liposomes as pharmaceutical carriers. <span><span class="ref-journal">Nat Rev Drug Discov. </span>2005;<span class="ref-vol">
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<strong>4</strong>
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</span>(2):145–60.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/15688077" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15688077</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>8.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.8">Storrs R.W. , Tropper F.D. , Li H.Y. , Song C.K. , Sipkins D.A. , Kuniyoshi J.K. , Bednarski M.D. , Strauss H.W. , Li K.C. Paramagnetic polymerized liposomes as new recirculating MR contrast agents. <span><span class="ref-journal">J Magn Reson Imaging. </span>1995;<span class="ref-vol">
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<strong>5</strong>
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</span>(6):719–24.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/8748492" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 8748492</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>9.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.9">Storrs R.W. , Tropper F.D. , Li H.Y. , Song C.K. , Kuniyoshi J.K. , Sipkins D.A. , Li C.P.K. , Bednarski M. Paramagnetic polymerized lyposomes: synthesis, characterization, and applications for magnetic resonance imaging. <span><span class="ref-journal">J. Am. Chem. Soc. </span>1995;<span class="ref-vol">
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<strong>117</strong>
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</span>:7301.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/8748492" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 8748492</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>10.</dt><dd><div class="bk_ref" id="ICAM_ACPLs.REF.10">Mulder W.J. , Strijkers G.J. , Griffioen A.W. , van Bloois L. , Molema G. , Storm G. , Koning G.A. , Nicolay K. A liposomal system for contrast-enhanced magnetic resonance imaging of molecular targets. <span><span class="ref-journal">Bioconjug Chem. </span>2004;<span class="ref-vol">
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<strong>15</strong>
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</span>(4):799–806.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/15264867" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15264867</span></a>]</div></dd></dl></dl></div><div id="bk_toc_contnr"></div></div></div><div class="fm-sec"><h2 id="_NBK23552_pubdet_">Publication Details</h2><h3>Author Information and Affiliations</h3><div class="contrib half_rhythm"><span itemprop="author">Huiming Zhang</span>, PhD<div class="affiliation small">
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National Center for Biotechnology Information, NLM, NIH, Bethesda, MD,
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<span class="before-email-separator"></span><span class="email-label">Email: </span><a href="mailto:dev@null" data-email="vog.hin.mln.ibcn@dacim" class="oemail">vog.hin.mln.ibcn@dacim</a>
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</div></div><h3>Publication History</h3><p class="small">Created: <span itemprop="datePublished">January 3, 2008</span>; Last Update: <span itemprop="dateModified">February 14, 2008</span>.</p><h3>Copyright</h3><div><div class="half_rhythm"><a href="/books/about/copyright/">Copyright Notice</a></div></div><h3>Publisher</h3><p><a href="http://www.ncbi.nlm.nih.gov/" ref="pagearea=page-banner&targetsite=external&targetcat=link&targettype=publisher">National Center for Biotechnology Information (US)</a>, Bethesda (MD)</p><h3>NLM Citation</h3><p>Zhang H. Anti-ICAM-1 antibody-conjugated paramagnetic liposomes. 2008 Jan 3 [Updated 2008 Feb 14]. In: Molecular Imaging and Contrast Agent Database (MICAD) [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2004-2013. <span class="bk_cite_avail"></span></p></div><div class="small-screen-prev"><a href="/books/n/micad/sosgadoliniumtexasred/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M75,30 c-80,60 -80,0 0,60 c-30,-60 -30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Prev</text></svg></a></div><div class="small-screen-next"><a href="/books/n/micad/sosgadoliniumgd3quantum/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M25,30c80,60 80,0 0,60 c30,-60 30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Next</text></svg></a></div></article><article data-type="table-wrap" id="figobICAMACPLsT1"><div id="ICAM_ACPLs.T1" class="table"><p class="large-table-link" style="display:none"><span class="right"><a href="/books/NBK23552/table/ICAM_ACPLs.T1/?report=objectonly" target="object">View in own window</a></span></p><div class="large_tbl" id="__ICAM_ACPLs.T1_lrgtbl__"><table><tbody><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Chemical name:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Anti-ICAM-1 antibody-conjugated paramagnetic liposomes</td><td rowspan="9" colspan="1" style="text-align:left;vertical-align:middle;"></td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Abbreviated name:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Anti-ICAM ACPLs</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Synonym:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;"></td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Agent category:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Antibody, small molecule (nanoparticle)</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Target:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">ICAM-1</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Target category:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Antigen</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Method of detection:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Magnetic resonance imaging (MRI), optical fluorescence microscopy</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Source of signal/contrast:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Gadolinium, Texas Red</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Activation:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">No</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Studies:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">
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<ul class="simple-list"><li class="half_rhythm"><div>
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<img alt="Checkbox" src="/corehtml/pmc/css/bookshelf/2.26/img/studies.checkbox.png" />
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<i>In vitro</i>
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</div></li></ul>
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<ul class="simple-list"><li class="half_rhythm"><div>
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<img alt="Checkbox" src="/corehtml/pmc/css/bookshelf/2.26/img/studies.checkbox.png" /> Rodents
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</div></li></ul>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">No structure is currently available in <a href="http://pubchem.ncbi.nlm.nih.gov" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubChem</a>.</td></tr></tbody></table></div></div></article></div><div id="jr-scripts"><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/libs.min.js"> </script><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/jr.min.js"> </script></div></div>
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