HTML Microdata document

This HTML5 document contains 2183 embedded RDF statements represented using HTML+Microdata notation.

The embedded RDF content will be recognized by any processor of HTML5 Microdata.

Namespace Prefixes

Prefix	IRI
dc	http://purl.org/dc/elements/1.1/
n2	http://purl.jp/bio/10/colil/ontology/201303#
n8	http://dx.doi.org/
rdfs	http://www.w3.org/2000/01/rdf-schema#
n9	http://togows.dbcls.jp/entry/pubmed/
xsdh	http://www.w3.org/2001/XMLSchema#
rdf	http://www.w3.org/1999/02/22-rdf-syntax-ns#
bibo	http://purl.org/ontology/bibo/
n3	http://purl.jp/bio/10/colil/id/
n5	http://purl.org/spar/doco/
n11	http://pubannotation.org/docs/sourcedb/PMC/sourceid/
n10	http://www.ncbi.nlm.nih.gov/pmc/articles/

Statements

Subject Item: n3:22754527
rdf:type: n2:CitationPaper n2:RelevantPaper n2:ReferencePaper
rdfs:seeAlso: n8:10.3389%2Ffphar.2012.00121 n9:22754527 n10:0 n11:0
bibo:cites: n3:11906799 n3:11570649 n3:20950334 n3:19486302 n3:19781861 n3:15708626 n3:19654589 n3:15051802 n3:1420090 n3:21979424 n3:10665489 n3:21641584 n3:14662518 n3:11271377 n3:14612135 n3:16174793 n3:8521001 n3:10864098 n3:16808729 n3:18773954 n3:12153997 n3:20976166 n3:16204638 n3:12531232 n3:18958626 n3:14614914 n3:16251831 n3:11519485 n3:19897075 n3:1521035 n3:10219256 n3:19897082 n3:1460864 n3:19533601 n3:14724353 n3:15100718 n3:12379911 n3:9242352 n3:16036808 n3:10103078 n3:10202832 n3:7505315 n3:11577244 n3:20624003 n3:21040844 n3:19162338 n3:11893586 n3:15228153 n3:21794992 n3:6106905 n3:8787655 n3:17689566 n3:12971663 n3:15708958 n3:9769913 n3:16498507 n3:9372455 n3:17034766 n3:15516806 n3:7242115 n3:21803344 n3:15494156 n3:20931246 n3:9106236 n3:1802127 n3:8147886 n3:17897974 n3:19077110 n3:16952162 n3:15910762 n3:11904622 n3:18991857 n3:18991854 n3:18991870 n3:19889792 n3:8874629 n3:17767502 n3:17105901 n3:17105918 n3:10065903 n3:16085522 n3:7651475 n3:19295339 n3:19742171 n3:18329007 n3:4023719 n3:19440461 n3:15189347 n3:19537954 n3:16670229 n3:16923848 n3:18606182 n3:19664713 n3:20849327 n3:16338084 n3:19890265 n3:11311463 n3:15135564 n3:20074221 n3:10482270 n3:22007835 n3:18638703 n3:18060582 n3:2454332 n3:17920942 n3:19659460 n3:20201849 n3:7378814 n3:9666272 n3:21333736 n3:8095976 n3:16796384 n3:16103774 n3:18580615 n3:9450229 n3:21595923 n3:19433117 n3:12053278 n3:9040492 n3:12174085 n3:22353781 n3:16165281 n3:20162563 n3:17992686 n3:18046654 n3:1356579 n3:2909798 n3:15579280 n3:18790057 n3:12421368 n3:15172778 n3:14982690 n3:21397004 n3:14982725 n3:17036005 n3:15955613 n3:15914466 n3:21766222 n3:11716818 n3:15677602 n3:10479471 n3:1984454 n3:12876559 n3:17597450 n3:11839560 n3:3543687 n3:21426580 n3:19271121 n3:9413272 n3:12394784 n3:21508219 n3:12434396 n3:20722969 n3:21239632 n3:16450214 n3:20188164 n3:21889975 n3:18970977 n3:15354631 n3:11865430 n3:9610668 n3:11071707 n3:15953347 n3:21272266 n3:9610683 n3:16881008 n3:18709468 n3:19374890 n3:15036625 n3:7658083 n3:18458095 n3:10560658
n2:cocitationWith: n3:21148086 n3:11309629 n3:24391808 n3:25644383 n3:20396973 n3:17914061 n3:21738771 n3:18430470 n3:56036 n3:15519244 n3:19654589 n3:11106749 n3:23084084 n3:25945248 n3:24267647 n3:10864098 n3:22048062 n3:1685745 n3:19506719 n3:16251831 n3:27402494 n3:18240064 n3:19897075 n3:16790532 n3:19897082 n3:20976166 n3:11519485 n3:19606280 n3:25268786 n3:16386305 n3:15977641 n3:21303698 n3:15962513 n3:14713949 n3:24424383 n3:19462243 n3:16036808 n3:21786077 n3:8728048 n3:24625401 n3:25377444 n3:21810934 n3:20624003 n3:21040844 n3:19364908 n3:10454636 n3:18305237 n3:25613133 n3:26539167 n3:17848967 n3:10358063 n3:24892744 n3:19630745 n3:16557263 n3:10822328 n3:22316499 n3:25999807 n3:12438433 n3:19738171 n3:20517932 n3:12684743 n3:22551810 n3:18265929 n3:23039106 n3:11724929 n3:15207256 n3:20492508 n3:21174240 n3:28441414 n3:12707054 n3:26661236 n3:16644490 n3:23721877 n3:8258759 n3:18991854 n3:8809853 n3:9498303 n3:17105918 n3:25529562 n3:18991959 n3:25209871 n3:22947176 n3:22820108 n3:10618285 n3:21219914 n3:25973614 n3:19306229 n3:19025481 n3:22714667 n3:1574543 n3:20668216 n3:2820058 n3:20953917 n3:1746528 n3:24486327 n3:19743454 n3:18941231 n3:21900636 n3:16153175 n3:28344073 n3:21792905 n3:23251514 n3:11729018 n3:23547924 n3:22591363 n3:16685256 n3:19287189 n3:18215617 n3:20201848 n3:25862193 n3:25788874 n3:21399909 n3:24867611 n3:23079813 n3:9666272 n3:24359561 n3:19233481 n3:21595923 n3:18509037 n3:18046654 n3:23456305 n3:25873042 n3:1604712 n3:22817991 n3:19319745 n3:2909798 n3:9278385 n3:28851615 n3:24894206 n3:15914466 n3:10602399 n3:15976090 n3:14982725 n3:15808355 n3:17976544 n3:26283916 n3:22934772 n3:21426580 n3:19543960 n3:8011238 n3:12551932 n3:21508219 n3:11754990 n3:25175865 n3:25175867 n3:25691383 n3:18709468 n3:16796601 n3:16086684 n3:18097880 n3:11865430 n3:15036625 n3:10550317
n2:hasRelevantBibliographicResourceOf: _:vb497081526 _:vb497081527 _:vb497081532 _:vb497081533 _:vb497081534 _:vb497081535 _:vb497081528 _:vb497081529 _:vb497081530 _:vb497081531 _:vb497081572 _:vb497081573 _:vb497081574 _:vb497081575 _:vb497081568 _:vb497081569 _:vb497081570 _:vb497081571 _:vb497081580 _:vb497081581 _:vb497081582 _:vb497081583 _:vb497081576 _:vb497081577 _:vb497081578 _:vb497081579 _:vb497081588 _:vb497081589 _:vb497081590 _:vb497081591 _:vb497081584 _:vb497081585 _:vb497081586 _:vb497081587 _:vb497081596 _:vb497081597 _:vb497081598 _:vb497081599 _:vb497081592 _:vb497081593 _:vb497081594 _:vb497081595 _:vb497081540 _:vb497081541 _:vb497081542 _:vb497081543 _:vb497081536 _:vb497081537 _:vb497081538 _:vb497081539 _:vb497081548 _:vb497081549 _:vb497081550 _:vb497081551 _:vb497081544 _:vb497081545 _:vb497081546 _:vb497081547 _:vb497081556 _:vb497081557 _:vb497081558 _:vb497081559 _:vb497081552 _:vb497081553 _:vb497081554 _:vb497081555 _:vb497081564 _:vb497081565 _:vb497081566 _:vb497081567 _:vb497081560 _:vb497081561 _:vb497081562 _:vb497081563 _:vb497081636 _:vb497081637 _:vb497081638 _:vb497081639 _:vb497081632 _:vb497081633 _:vb497081634 _:vb497081635 _:vb497081644 _:vb497081645 _:vb497081646 _:vb497081647 _:vb497081640 _:vb497081641 _:vb497081642 _:vb497081643 _:vb497081652 _:vb497081653 _:vb497081654 _:vb497081655 _:vb497081648 _:vb497081649 _:vb497081650 _:vb497081651 _:vb497081660 _:vb497081661 _:vb497081662 _:vb497081663 _:vb497081656 _:vb497081657 _:vb497081658 _:vb497081659 _:vb497081604 _:vb497081605 _:vb497081606 _:vb497081607 _:vb497081600 _:vb497081601 _:vb497081602 _:vb497081603 _:vb497081612 _:vb497081613 _:vb497081614 _:vb497081615 _:vb497081608 _:vb497081609 _:vb497081610 _:vb497081611 _:vb497081620 _:vb497081621 _:vb497081622 _:vb497081623 _:vb497081616 _:vb497081617 _:vb497081618 _:vb497081619 _:vb497081628 _:vb497081629 _:vb497081630 _:vb497081631 _:vb497081624 _:vb497081625 _:vb497081626 _:vb497081627 _:vb497081668 _:vb497081669 _:vb497081670 _:vb497081671 _:vb497081664 _:vb497081665 _:vb497081666 _:vb497081667 _:vb497081676 _:vb497081677 _:vb497081678 _:vb497081672 _:vb497081673 _:vb497081674 _:vb497081675
n2:pmcid: PMC0
bibo:doi: 10.3389%2Ffphar.2012.00121
n5:contains: _:vb16821850 _:vb16821644 _:vb16821594

Subject Item: _:vb16821594
rdf:type: n5:Section
dc:title: introduction
n5:contains: _:vb16821640 _:vb16821641 _:vb16821642 _:vb16821643 _:vb16821636 _:vb16821637 _:vb16821638 _:vb16821639 _:vb16821632 _:vb16821633 _:vb16821634 _:vb16821635 _:vb16821596 _:vb16821597 _:vb16821598 _:vb16821599 _:vb16821595 _:vb16821612 _:vb16821613 _:vb16821614 _:vb16821615 _:vb16821608 _:vb16821609 _:vb16821610 _:vb16821611 _:vb16821604 _:vb16821605 _:vb16821606 _:vb16821607 _:vb16821600 _:vb16821601 _:vb16821602 _:vb16821603 _:vb16821628 _:vb16821629 _:vb16821630 _:vb16821631 _:vb16821624 _:vb16821625 _:vb16821626 _:vb16821627 _:vb16821620 _:vb16821621 _:vb16821622 _:vb16821623 _:vb16821616 _:vb16821617 _:vb16821618 _:vb16821619

Subject Item: _:vb16821595
rdf:type: n2:Context
rdf:value: The blood brain barrier (BBB) is a specialized structure formed by brain endothelial cells (BECs) that are tightly interconnected to form a boundary between the central nervous system (CNS) and periphery (Abbott et al., >>2010<<). Once thought to be static, the BBB is now known to be an active and dynamic interface that responds to signals from both the brain parenchyma and vasculature.
n2:mentions: n3:19664713

Subject Item: _:vb16821596
rdf:type: n2:Context
rdf:value: BBB dysfunction contributes to the pathophysiology of numerous CNS disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, ischemia, and neuroAIDS (Stewart et al., >>1992<<; Nath et al., 2001; Samii et al., 2004; Compston and Coles, 2008; Yenari and Han, 2012).
n2:mentions: n3:1460864

Subject Item: _:vb16821597
rdf:type: n2:Context
rdf:value: BBB dysfunction contributes to the pathophysiology of numerous CNS disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, ischemia, and neuroAIDS (Stewart et al., 1992; Nath et al., >>2001<<; Samii et al., 2004; Compston and Coles, 2008; Yenari and Han, 2012).
n2:mentions: n3:11519485

Subject Item: _:vb16821598
rdf:type: n2:Context
rdf:value: dysfunction contributes to the pathophysiology of numerous CNS disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, ischemia, and neuroAIDS (Stewart et al., 1992; Nath et al., 2001; Samii et al., >>2004<<; Compston and Coles, 2008; Yenari and Han, 2012). Recent evidence points to the ability of drugs of abuse (e.g., stimulants) to disrupt BBB function.
n2:mentions: n3:15172778

Subject Item: _:vb16821599
rdf:type: n2:Context
rdf:value: the pathophysiology of numerous CNS disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, ischemia, and neuroAIDS (Stewart et al., 1992; Nath et al., 2001; Samii et al., 2004; Compston and Coles, >>2008<<; Yenari and Han, 2012). Recent evidence points to the ability of drugs of abuse (e.g., stimulants) to disrupt BBB function.
n2:mentions: n3:18970977

Subject Item: _:vb16821600
rdf:type: n2:Context
rdf:value: numerous CNS disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, ischemia, and neuroAIDS (Stewart et al., 1992; Nath et al., 2001; Samii et al., 2004; Compston and Coles, 2008; Yenari and Han, >>2012<<). Recent evidence points to the ability of drugs of abuse (e.g., stimulants) to disrupt BBB function.
n2:mentions: n3:22353781

Subject Item: _:vb16821601
rdf:type: n2:Context
rdf:value: The structure of the BBB has been thoroughly described in other reviews (Sandoval and Witt, >>2008<<; Carvey et al., 2009). In brief, the BBB is comprised of highly specialized BECs which interact with pericytes, the vascular basement membrane, and astrocytes (Diaz-Flores et al., 1991; Krueger and Bechmann, 2010).
n2:mentions: n3:18790057

Subject Item: _:vb16821602
rdf:type: n2:Context
rdf:value: The structure of the BBB has been thoroughly described in other reviews (Sandoval and Witt, 2008; Carvey et al., >>2009<<). In brief, the BBB is comprised of highly specialized BECs which interact with pericytes, the vascular basement membrane, and astrocytes (Diaz-Flores et al., 1991; Krueger and Bechmann, 2010).
n2:mentions: n3:19659460

Subject Item: _:vb16821603
rdf:type: n2:Context
rdf:value: In brief, the BBB is comprised of highly specialized BECs which interact with pericytes, the vascular basement membrane, and astrocytes (Diaz-Flores et al., >>1991<<; Krueger and Bechmann, 2010).
n2:mentions: n3:1802127

Subject Item: _:vb16821604
rdf:type: n2:Context
rdf:value: In brief, the BBB is comprised of highly specialized BECs which interact with pericytes, the vascular basement membrane, and astrocytes (Diaz-Flores et al., 1991; Krueger and Bechmann, >>2010<<). BECs are closely associated through cell–cell complexes of tight junction proteins: claudins, occludins, and junctional adhesion molecules (JAMs; Hawkins and Davis, 2005). Adherens junctions also form between BECs. Accessory proteins
n2:mentions: n3:19533601

Subject Item: _:vb16821605
rdf:type: n2:Context
rdf:value: BECs are closely associated through cell–cell complexes of tight junction proteins: claudins, occludins, and junctional adhesion molecules (JAMs; Hawkins and Davis, >>2005<<). Adherens junctions also form between BECs. Accessory proteins like zona occludins (ZO), cingulin, and afadin (AF-6) provide structural support and stability to both tight and adherens junctions (Yamamoto et al., 1999; Mark and Davis,
n2:mentions: n3:15914466

Subject Item: _:vb16821606
rdf:type: n2:Context
rdf:value: Accessory proteins like zona occludins (ZO), cingulin, and afadin (AF-6) provide structural support and stability to both tight and adherens junctions (Yamamoto et al., >>1999<<; Mark and Davis, 2002).
n2:mentions: n3:10103078

Subject Item: _:vb16821607
rdf:type: n2:Context
rdf:value: Accessory proteins like zona occludins (ZO), cingulin, and afadin (AF-6) provide structural support and stability to both tight and adherens junctions (Yamamoto et al., 1999; Mark and Davis, >>2002<<). Though little is known about pericyte involvement within the BBB, these cells likely regulate cerebral blood flow (Bandopadhyay et al., 2001) and stabilize forming vessels (Ramsauer et al., 2002). BECs and pericytes are enveloped by
n2:mentions: n3:11893586

Subject Item: _:vb16821608
rdf:type: n2:Context
rdf:value: Though little is known about pericyte involvement within the BBB, these cells likely regulate cerebral blood flow (Bandopadhyay et al., >>2001<<) and stabilize forming vessels (Ramsauer et al., 2002).
n2:mentions: n3:11577244

Subject Item: _:vb16821609
rdf:type: n2:Context
rdf:value: Though little is known about pericyte involvement within the BBB, these cells likely regulate cerebral blood flow (Bandopadhyay et al., 2001) and stabilize forming vessels (Ramsauer et al., >>2002<<). BECs and pericytes are enveloped by extracellular matrix proteins that comprise the basement membrane (Farkas and Luiten, 2001). Astrocytes interact with components of the BBB through their foot processes that make contact with BECs to
n2:mentions: n3:12153997

Subject Item: _:vb16821610
rdf:type: n2:Context
rdf:value: BECs and pericytes are enveloped by extracellular matrix proteins that comprise the basement membrane (Farkas and Luiten, >>2001<<). Astrocytes interact with components of the BBB through their foot processes that make contact with BECs to form the glia limitans perivascularis as well as the basement membrane (Krueger and Bechmann, 2010). Astrocytic foot process in
n2:mentions: n3:11311463

Subject Item: _:vb16821611
rdf:type: n2:Context
rdf:value: Astrocytes interact with components of the BBB through their foot processes that make contact with BECs to form the glia limitans perivascularis as well as the basement membrane (Krueger and Bechmann, >>2010<<). Astrocytic foot process in the margin of the brain form a thin membrane called the glia limitans superficialis in the subarachnoid space. These two glia limitans are classically viewed as continuous, starting at the subarachnoid space,
n2:mentions: n3:19533601

Subject Item: _:vb16821612
rdf:type: n2:Context
rdf:value: Astrocytes facilitate BBB development by inducing tight junction formation, providing microvascular support, and allowing molecule (e.g., water, sugar, ions) diffusion into the brain (Janzer and Raff, >>1987<<; Madsen and Hirschberg, 2010).
n2:mentions: n3:3543687

Subject Item: _:vb16821613
rdf:type: n2:Context
rdf:value: Astrocytes facilitate BBB development by inducing tight junction formation, providing microvascular support, and allowing molecule (e.g., water, sugar, ions) diffusion into the brain (Janzer and Raff, 1987; Madsen and Hirschberg, >>2010<<).
n2:mentions: n3:20162563

Subject Item: _:vb16821614
rdf:type: n2:Context
rdf:value: These interactions are promoted by the BBB, neurons, and glia, which together make up the neuro(glio)vascular unit (Hawkins and Davis, >>2005<<; Koehler et al., 2009).
n2:mentions: n3:15914466

Subject Item: _:vb16821615
rdf:type: n2:Context
rdf:value: These interactions are promoted by the BBB, neurons, and glia, which together make up the neuro(glio)vascular unit (Hawkins and Davis, 2005; Koehler et al., >>2009<<). This neurovascular coupling regulates cerebral blood flow enabling efficient oxygen and nutrient supply to various cell types and brain regions (Iadecola, 2004). Moreover, intracellular communication within the neuro(glio)vascular unit
n2:mentions: n3:19162338

Subject Item: _:vb16821616
rdf:type: n2:Context
rdf:value: This neurovascular coupling regulates cerebral blood flow enabling efficient oxygen and nutrient supply to various cell types and brain regions (Iadecola, >>2004<<). Moreover, intracellular communication within the neuro(glio)vascular unit allows for localized control of cerebral blood flow to match the needs of specific brain regions. These interactions are important for blood flow to the neurons,
n2:mentions: n3:15100718

Subject Item: _:vb16821617
rdf:type: n2:Context
rdf:value: These toxins may be endogenous factors or exogenous xenobiotics (Abbott et al., >>2010<<). The impenetrability of the BBB results from physical restriction due to tight junction connectivity of BECs, transport regulation limiting transcellular migration, and enzymatic activities of BECs that metabolize harmful substances at
n2:mentions: n3:19664713

Subject Item: _:vb16821618
rdf:type: n2:Context
rdf:value: restriction due to tight junction connectivity of BECs, transport regulation limiting transcellular migration, and enzymatic activities of BECs that metabolize harmful substances at the vascular face of the BBB (Madsen and Hirschberg, >>2010<<).
n2:mentions: n3:20162563

Subject Item: _:vb16821619
rdf:type: n2:Context
rdf:value: within the BBB are numerous, but in general, transporters can be categorized as being ion transporters, active transporters (e.g., P-glycoprotein), sodium-dependent transporters, or sodium-independent transporters (Carvey et al., >>2009<<). These transport systems supply nutrients to the brain from the blood and remove metabolic byproducts from the brain to the blood for elimination (Ohtsuki, 2004).
n2:mentions: n3:19659460

Subject Item: _:vb16821620
rdf:type: n2:Context
rdf:value: These transport systems supply nutrients to the brain from the blood and remove metabolic byproducts from the brain to the blood for elimination (Ohtsuki, >>2004<<).
n2:mentions: n3:15516806

Subject Item: _:vb16821621
rdf:type: n2:Context
rdf:value: Contractile proteins identified in pericytes are thought to alter vascular diameter and cerebrovascular blood flow (Bandopadhyay et al., >>2001<<). Transport systems bring in vasoactive factors from the periphery that interact with smooth muscle cells and pericytes surrounding the BBB endothelium to allow for vasodilation or constriction (Peppiatt et al., 2006; Bell et al., 2010).
n2:mentions: n3:11577244

Subject Item: _:vb16821622
rdf:type: n2:Context
rdf:value: Transport systems bring in vasoactive factors from the periphery that interact with smooth muscle cells and pericytes surrounding the BBB endothelium to allow for vasodilation or constriction (Peppiatt et al., >>2006<<; Bell et al., 2010).
n2:mentions: n3:17036005

Subject Item: _:vb16821623
rdf:type: n2:Context
rdf:value: Transport systems bring in vasoactive factors from the periphery that interact with smooth muscle cells and pericytes surrounding the BBB endothelium to allow for vasodilation or constriction (Peppiatt et al., 2006; Bell et al., >>2010<<). Additionally, cells within the neuro(glio)vascular unit can secrete local vasoregulators like norepinephrine, nitric oxide, and endothelin which regulate regional cerebral blood flow (Lecrux and Hamel, 2011).
n2:mentions: n3:21040844

Subject Item: _:vb16821624
rdf:type: n2:Context
rdf:value: Additionally, cells within the neuro(glio)vascular unit can secrete local vasoregulators like norepinephrine, nitric oxide, and endothelin which regulate regional cerebral blood flow (Lecrux and Hamel, >>2011<<).
n2:mentions: n3:21272266

Subject Item: _:vb16821625
rdf:type: n2:Context
rdf:value: However, select leukocytes like neutrophils, can cross the BBB during normal immune surveillance with little disruption to BBB tight junctions (Petty and Lo, >>2002<<). During a neuroinflammatory response, immune factors, and endothelial adhesion molecules signal to increase immune cell migration through the BBB (Petty and Lo, 2002). Signals resulting in increased immune cell migration can alter the
n2:mentions: n3:12531232

Subject Item: _:vb16821626
rdf:type: n2:Context
rdf:value: During a neuroinflammatory response, immune factors, and endothelial adhesion molecules signal to increase immune cell migration through the BBB (Petty and Lo, >>2002<<). Signals resulting in increased immune cell migration can alter the structural organization of tight junction proteins and lead to actin cytoskeleton remodeling in the BBB basement membrane (Deli et al., 1995; Couraud, 1998; Ransohoff et
n2:mentions: n3:12531232

Subject Item: _:vb16821627
rdf:type: n2:Context
rdf:value: Signals resulting in increased immune cell migration can alter the structural organization of tight junction proteins and lead to actin cytoskeleton remodeling in the BBB basement membrane (Deli et al., >>1995<<; Couraud, 1998; Ransohoff et al., 2003).
n2:mentions: n3:8521001

Subject Item: _:vb16821628
rdf:type: n2:Context
rdf:value: Signals resulting in increased immune cell migration can alter the structural organization of tight junction proteins and lead to actin cytoskeleton remodeling in the BBB basement membrane (Deli et al., 1995; Couraud, >>1998<<; Ransohoff et al., 2003).
n2:mentions: n3:9769913

Subject Item: _:vb16821629
rdf:type: n2:Context
rdf:value: resulting in increased immune cell migration can alter the structural organization of tight junction proteins and lead to actin cytoskeleton remodeling in the BBB basement membrane (Deli et al., 1995; Couraud, 1998; Ransohoff et al., >>2003<<). Migrating peripheral immune cells disrupt normal BBB function, and produce cytokines and chemokines within the CNS which furthers BBB disruption (Cartier et al., 2005).
n2:mentions: n3:12876559

Subject Item: _:vb16821630
rdf:type: n2:Context
rdf:value: Migrating peripheral immune cells disrupt normal BBB function, and produce cytokines and chemokines within the CNS which furthers BBB disruption (Cartier et al., >>2005<<). Cytokines [e.g., tumor necrosis factor alpha (TNFα), interleukin (IL)-1β and IL-6] and the CCL2 chemokine are increased in serum, neuronal tissue, and cerebrospinal fluid in several CNS disorders including traumatic brain injury
n2:mentions: n3:15708626

Subject Item: _:vb16821631
rdf:type: n2:Context
rdf:value: necrosis factor alpha (TNFα), interleukin (IL)-1β and IL-6] and the CCL2 chemokine are increased in serum, neuronal tissue, and cerebrospinal fluid in several CNS disorders including traumatic brain injury (Morganti-Kossman et al., >>1997<<), HIV-associated encephalitis (Cartier et al., 2005), and Huntington disease (Stolp and Dziegielewska, 2009).
n2:mentions: n3:9106236

Subject Item: _:vb16821632
rdf:type: n2:Context
rdf:value: and IL-6] and the CCL2 chemokine are increased in serum, neuronal tissue, and cerebrospinal fluid in several CNS disorders including traumatic brain injury (Morganti-Kossman et al., 1997), HIV-associated encephalitis (Cartier et al., >>2005<<), and Huntington disease (Stolp and Dziegielewska, 2009). These neuroinflammatory factors likely contribute to BBB breakdown occurring in these disorders through activity at their receptors on BECs and other BBB cell types (Buckner et al.
n2:mentions: n3:15708626

Subject Item: _:vb16821633
rdf:type: n2:Context
rdf:value: neuronal tissue, and cerebrospinal fluid in several CNS disorders including traumatic brain injury (Morganti-Kossman et al., 1997), HIV-associated encephalitis (Cartier et al., 2005), and Huntington disease (Stolp and Dziegielewska, >>2009<<). These neuroinflammatory factors likely contribute to BBB breakdown occurring in these disorders through activity at their receptors on BECs and other BBB cell types (Buckner et al., 2006).
n2:mentions: n3:19077110

Subject Item: _:vb16821634
rdf:type: n2:Context
rdf:value: These neuroinflammatory factors likely contribute to BBB breakdown occurring in these disorders through activity at their receptors on BECs and other BBB cell types (Buckner et al., >>2006<<). Peripheral immune cells can also trigger increased production of inflammatory factors (Verma and Szmitko, 2006; Fletcher et al., 2009), neurotransmitters (e.g., glutamate), neurotrophic factors (e.g., vascular endothelial growth
n2:mentions: n3:16923848

Subject Item: _:vb16821635
rdf:type: n2:Context
rdf:value: Peripheral immune cells can also trigger increased production of inflammatory factors (Verma and Szmitko, >>2006<<; Fletcher et al., 2009), neurotransmitters (e.g., glutamate), neurotrophic factors (e.g., vascular endothelial growth factor), and proteases (e.g., matrix metallopeptidase (MMP-9; Petty and Lo, 2002) from BECs and astrocytes.
n2:mentions: n3:16498507

Subject Item: _:vb16821636
rdf:type: n2:Context
rdf:value: Peripheral immune cells can also trigger increased production of inflammatory factors (Verma and Szmitko, 2006; Fletcher et al., >>2009<<), neurotransmitters (e.g., glutamate), neurotrophic factors (e.g., vascular endothelial growth factor), and proteases (e.g., matrix metallopeptidase (MMP-9; Petty and Lo, 2002) from BECs and astrocytes.
n2:mentions: n3:19486302

Subject Item: _:vb16821637
rdf:type: n2:Context
rdf:value: factors (Verma and Szmitko, 2006; Fletcher et al., 2009), neurotransmitters (e.g., glutamate), neurotrophic factors (e.g., vascular endothelial growth factor), and proteases (e.g., matrix metallopeptidase (MMP-9; Petty and Lo, >>2002<<) from BECs and astrocytes. These factors perpetuate neuroinflammation, and contribute to continuing alterations to the BBB (Petty and Lo, 2002).
n2:mentions: n3:12531232

Subject Item: _:vb16821638
rdf:type: n2:Context
rdf:value: These factors perpetuate neuroinflammation, and contribute to continuing alterations to the BBB (Petty and Lo, >>2002<<). Alterations in BBB integrity resulting from neuroinflammation produce a cascade resulting in further BBB disruption and increased penetration of immune cells into the CNS. This feed-forward cycle can lead to disruptions in physiological
n2:mentions: n3:12531232

Subject Item: _:vb16821639
rdf:type: n2:Context
rdf:value: This may accelerate the onset of the neurotoxicities associated with chronic use of these potent drugs (Czub et al., >>2001<<; Nath et al., 2002).
n2:mentions: n3:11271377

Subject Item: _:vb16821640
rdf:type: n2:Context
rdf:value: This may accelerate the onset of the neurotoxicities associated with chronic use of these potent drugs (Czub et al., 2001; Nath et al., >>2002<<). This review focuses on the effects of psychostimulant drugs though many of the molecular and cellular mechanisms of BBB dysfunction and neuroinflammation have been well-characterized in studies focused on the CNS depressant alcohol (see
n2:mentions: n3:12394784

Subject Item: _:vb16821641
rdf:type: n2:Context
rdf:value: of psychostimulant drugs though many of the molecular and cellular mechanisms of BBB dysfunction and neuroinflammation have been well-characterized in studies focused on the CNS depressant alcohol (see reviews: de la Monte et al., >>2009<<; Perdisky et al., 2011; Strazza et al., 2011).
n2:mentions: n3:19742171

Subject Item: _:vb16821642
rdf:type: n2:Context
rdf:value: drugs though many of the molecular and cellular mechanisms of BBB dysfunction and neuroinflammation have been well-characterized in studies focused on the CNS depressant alcohol (see reviews: de la Monte et al., 2009; Perdisky et al., >>2011<<; Strazza et al., 2011).
n2:mentions: n3:21397004

Subject Item: _:vb16821643
rdf:type: n2:Context
rdf:value: molecular and cellular mechanisms of BBB dysfunction and neuroinflammation have been well-characterized in studies focused on the CNS depressant alcohol (see reviews: de la Monte et al., 2009; Perdisky et al., 2011; Strazza et al., >>2011<<).
n2:mentions: n3:21641584

Subject Item: _:vb16821644
rdf:type: n5:Section
dc:title: stimulant drugs and the bbb
n5:contains: _:vb16821716 _:vb16821717 _:vb16821718 _:vb16821719 _:vb16821712 _:vb16821713 _:vb16821714 _:vb16821715 _:vb16821724 _:vb16821725 _:vb16821726 _:vb16821727 _:vb16821720 _:vb16821721 _:vb16821722 _:vb16821723 _:vb16821700 _:vb16821701 _:vb16821702 _:vb16821703 _:vb16821696 _:vb16821697 _:vb16821698 _:vb16821699 _:vb16821708 _:vb16821709 _:vb16821710 _:vb16821711 _:vb16821704 _:vb16821705 _:vb16821706 _:vb16821707 _:vb16821748 _:vb16821749 _:vb16821750 _:vb16821751 _:vb16821744 _:vb16821745 _:vb16821746 _:vb16821747 _:vb16821756 _:vb16821757 _:vb16821758 _:vb16821759 _:vb16821752 _:vb16821753 _:vb16821754 _:vb16821755 _:vb16821732 _:vb16821733 _:vb16821734 _:vb16821735 _:vb16821728 _:vb16821729 _:vb16821730 _:vb16821731 _:vb16821740 _:vb16821741 _:vb16821742 _:vb16821743 _:vb16821736 _:vb16821737 _:vb16821738 _:vb16821739 _:vb16821652 _:vb16821653 _:vb16821654 _:vb16821655 _:vb16821648 _:vb16821649 _:vb16821650 _:vb16821651 _:vb16821660 _:vb16821661 _:vb16821662 _:vb16821663 _:vb16821656 _:vb16821657 _:vb16821658 _:vb16821659 _:vb16821645 _:vb16821646 _:vb16821647 _:vb16821684 _:vb16821685 _:vb16821686 _:vb16821687 _:vb16821680 _:vb16821681 _:vb16821682 _:vb16821683 _:vb16821692 _:vb16821693 _:vb16821694 _:vb16821695 _:vb16821688 _:vb16821689 _:vb16821690 _:vb16821691 _:vb16821668 _:vb16821669 _:vb16821670 _:vb16821671 _:vb16821664 _:vb16821665 _:vb16821666 _:vb16821667 _:vb16821676 _:vb16821677 _:vb16821678 _:vb16821679 _:vb16821672 _:vb16821673 _:vb16821674 _:vb16821675 _:vb16821844 _:vb16821845 _:vb16821846 _:vb16821847 _:vb16821840 _:vb16821841 _:vb16821842 _:vb16821843 _:vb16821848 _:vb16821849 _:vb16821828 _:vb16821829 _:vb16821830 _:vb16821831 _:vb16821824 _:vb16821825 _:vb16821826 _:vb16821827 _:vb16821836 _:vb16821837 _:vb16821838 _:vb16821839 _:vb16821832 _:vb16821833 _:vb16821834 _:vb16821835 _:vb16821780 _:vb16821781 _:vb16821782 _:vb16821783 _:vb16821776 _:vb16821777 _:vb16821778 _:vb16821779 _:vb16821788 _:vb16821789 _:vb16821790 _:vb16821791 _:vb16821784 _:vb16821785 _:vb16821786 _:vb16821787 _:vb16821764 _:vb16821765 _:vb16821766 _:vb16821767 _:vb16821760 _:vb16821761 _:vb16821762 _:vb16821763 _:vb16821772 _:vb16821773 _:vb16821774 _:vb16821775 _:vb16821768 _:vb16821769 _:vb16821770 _:vb16821771 _:vb16821812 _:vb16821813 _:vb16821814 _:vb16821815 _:vb16821808 _:vb16821809 _:vb16821810 _:vb16821811 _:vb16821820 _:vb16821821 _:vb16821822 _:vb16821823 _:vb16821816 _:vb16821817 _:vb16821818 _:vb16821819 _:vb16821796 _:vb16821797 _:vb16821798 _:vb16821799 _:vb16821792 _:vb16821793 _:vb16821794 _:vb16821795 _:vb16821804 _:vb16821805 _:vb16821806 _:vb16821807 _:vb16821800 _:vb16821801 _:vb16821802 _:vb16821803

Subject Item: _:vb16821645
rdf:type: n2:Context
rdf:value: Meth reverses the transport of norepinephrine, dopamine (DA), and serotonin (5-HT) leading to excess release of these monoamines from the cytoplasm and storage vesicles into the synapse (Rothman et al., >>2001<<). Meth also prevents monoamine reuptake causing them to remain in the synaptic cleft to increase post-synaptic receptor stimulation. Chronic meth abuse in humans is associated with neurotoxicities resulting in damage to both DA and 5-HT
n2:mentions: n3:11071707

Subject Item: _:vb16821646
rdf:type: n2:Context
rdf:value: Proposed mechanisms underlying meth-induced neurotoxicity include increased reactive oxygen species (ROS) and dopamine-quinone (DAQ) production (Kuhn et al., >>2006<<), hyperthermia (Kiyatkin et al., 2007), neuroinflammation (Guilarte et al., 2003), and BBB dysfunction (Sharma and Kiyatkin, 2009).
n2:mentions: n3:17105901

Subject Item: _:vb16821647
rdf:type: n2:Context
rdf:value: Proposed mechanisms underlying meth-induced neurotoxicity include increased reactive oxygen species (ROS) and dopamine-quinone (DAQ) production (Kuhn et al., 2006), hyperthermia (Kiyatkin et al., >>2007<<), neuroinflammation (Guilarte et al., 2003), and BBB dysfunction (Sharma and Kiyatkin, 2009).
n2:mentions: n3:17767502

Subject Item: _:vb16821648
rdf:type: n2:Context
rdf:value: mechanisms underlying meth-induced neurotoxicity include increased reactive oxygen species (ROS) and dopamine-quinone (DAQ) production (Kuhn et al., 2006), hyperthermia (Kiyatkin et al., 2007), neuroinflammation (Guilarte et al., >>2003<<), and BBB dysfunction (Sharma and Kiyatkin, 2009).
n2:mentions: n3:14614914

Subject Item: _:vb16821649
rdf:type: n2:Context
rdf:value: include increased reactive oxygen species (ROS) and dopamine-quinone (DAQ) production (Kuhn et al., 2006), hyperthermia (Kiyatkin et al., 2007), neuroinflammation (Guilarte et al., 2003), and BBB dysfunction (Sharma and Kiyatkin, >>2009<<). It is likely that more than one mechanism underlies the neuronal maladaptations and damage associated with meth abuse, and that this damage is associated with the interaction of multiple mechanisms.
n2:mentions: n3:18773954

Subject Item: _:vb16821650
rdf:type: n2:Context
rdf:value: For example, oxidative stress and hyperthermia can increase BBB dysfunction which in turn, can exacerbate neuroinflammation after meth exposure. While some studies show direct neurotoxicity (Ricaurte et al., >>1980<<; McCann et al., 2008) after meth exposure without BBB disruption or neuroinflammation, these studies did not assess changes in the BBB or in the inflammatory response so it is uncertain whether neurotoxicity can occur independent of BBB
n2:mentions: n3:7378814

Subject Item: _:vb16821651
rdf:type: n2:Context
rdf:value: While some studies show direct neurotoxicity (Ricaurte et al., 1980; McCann et al., >>2008<<) after meth exposure without BBB disruption or neuroinflammation, these studies did not assess changes in the BBB or in the inflammatory response so it is uncertain whether neurotoxicity can occur independent of BBB disruption and/or
n2:mentions: n3:17992686

Subject Item: _:vb16821652
rdf:type: n2:Context
rdf:value: injection of either 3 or 9 mg/kg meth in rats resulted in BBB damage in the prefrontal cortex and nucleus accumbens shell, identified by punctate areas of fluorescein isothiocyanate (FITC)-labeled albumin leakage (Kousik et al., >>2011<<). Other rodent studies also showed BBB dysfunction following acute meth treatment marked by leakage of Evans blue into the parenchyma or through increased IgG immunostaining (Bowyer and Ali, 2006; Bowyer et al., 2008;Kiyatkin and Sharma,
n2:mentions: n3:21979424

Subject Item: _:vb16821653
rdf:type: n2:Context
rdf:value: Other rodent studies also showed BBB dysfunction following acute meth treatment marked by leakage of Evans blue into the parenchyma or through increased IgG immunostaining (Bowyer and Ali, >>2006<<; Bowyer et al., 2008;Kiyatkin and Sharma, 2009, 2011; Sharma and Kiyatkin, 2009; Kuroda et al., 2010; Martins et al., 2011).
n2:mentions: n3:16952162

Subject Item: _:vb16821654
rdf:type: n2:Context
rdf:value: Other rodent studies also showed BBB dysfunction following acute meth treatment marked by leakage of Evans blue into the parenchyma or through increased IgG immunostaining (Bowyer and Ali, 2006; Bowyer et al., >>2008<<;Kiyatkin and Sharma, 2009, 2011; Sharma and Kiyatkin, 2009; Kuroda et al., 2010; Martins et al., 2011).
n2:mentions: n3:18991857

Subject Item: _:vb16821655
rdf:type: n2:Context
rdf:value: rodent studies also showed BBB dysfunction following acute meth treatment marked by leakage of Evans blue into the parenchyma or through increased IgG immunostaining (Bowyer and Ali, 2006; Bowyer et al., 2008;Kiyatkin and Sharma, >>2009<<, 2011; Sharma and Kiyatkin, 2009; Kuroda et al., 2010; Martins et al., 2011). The treatment regimens varied greatly from single doses ranging from 3–40 mg/kg to several acute doses over 24 h, all of which compromised BBB integrity.
n2:mentions: n3:19897075

Subject Item: _:vb16821656
rdf:type: n2:Context
rdf:value: studies also showed BBB dysfunction following acute meth treatment marked by leakage of Evans blue into the parenchyma or through increased IgG immunostaining (Bowyer and Ali, 2006; Bowyer et al., 2008;Kiyatkin and Sharma, 2009, >>2011<<; Sharma and Kiyatkin, 2009; Kuroda et al., 2010; Martins et al., 2011). The treatment regimens varied greatly from single doses ranging from 3–40 mg/kg to several acute doses over 24 h, all of which compromised BBB integrity.
n2:mentions: n3:20931246

Subject Item: _:vb16821657
rdf:type: n2:Context
rdf:value: dysfunction following acute meth treatment marked by leakage of Evans blue into the parenchyma or through increased IgG immunostaining (Bowyer and Ali, 2006; Bowyer et al., 2008;Kiyatkin and Sharma, 2009, 2011; Sharma and Kiyatkin, >>2009<<; Kuroda et al., 2010; Martins et al., 2011). The treatment regimens varied greatly from single doses ranging from 3–40 mg/kg to several acute doses over 24 h, all of which compromised BBB integrity.
n2:mentions: n3:18773954

Subject Item: _:vb16821658
rdf:type: n2:Context
rdf:value: acute meth treatment marked by leakage of Evans blue into the parenchyma or through increased IgG immunostaining (Bowyer and Ali, 2006; Bowyer et al., 2008;Kiyatkin and Sharma, 2009, 2011; Sharma and Kiyatkin, 2009; Kuroda et al., >>2010<<; Martins et al., 2011). The treatment regimens varied greatly from single doses ranging from 3–40 mg/kg to several acute doses over 24 h, all of which compromised BBB integrity.
n2:mentions: n3:19890265

Subject Item: _:vb16821659
rdf:type: n2:Context
rdf:value: marked by leakage of Evans blue into the parenchyma or through increased IgG immunostaining (Bowyer and Ali, 2006; Bowyer et al., 2008;Kiyatkin and Sharma, 2009, 2011; Sharma and Kiyatkin, 2009; Kuroda et al., 2010; Martins et al., >>2011<<). The treatment regimens varied greatly from single doses ranging from 3–40 mg/kg to several acute doses over 24 h, all of which compromised BBB integrity.
n2:mentions: n3:21803344

Subject Item: _:vb16821660
rdf:type: n2:Context
rdf:value: changes in DA or 5-HT levels and terminal damage were most pronounced, including the striatum, cortex, and hippocampus, but not in areas where monoamine levels were unaffected by meth (e.g., the substantia nigra; Sharma and Ali, >>2006<<; Bowyer et al., 2008; Kousik et al., 2011; Martins et al., 2011).
n2:mentions: n3:17105918

Subject Item: _:vb16821661
rdf:type: n2:Context
rdf:value: 5-HT levels and terminal damage were most pronounced, including the striatum, cortex, and hippocampus, but not in areas where monoamine levels were unaffected by meth (e.g., the substantia nigra; Sharma and Ali, 2006; Bowyer et al., >>2008<<; Kousik et al., 2011; Martins et al., 2011).
n2:mentions: n3:18991857

Subject Item: _:vb16821662
rdf:type: n2:Context
rdf:value: damage were most pronounced, including the striatum, cortex, and hippocampus, but not in areas where monoamine levels were unaffected by meth (e.g., the substantia nigra; Sharma and Ali, 2006; Bowyer et al., 2008; Kousik et al., >>2011<<; Martins et al., 2011).
n2:mentions: n3:21979424

Subject Item: _:vb16821663
rdf:type: n2:Context
rdf:value: pronounced, including the striatum, cortex, and hippocampus, but not in areas where monoamine levels were unaffected by meth (e.g., the substantia nigra; Sharma and Ali, 2006; Bowyer et al., 2008; Kousik et al., 2011; Martins et al., >>2011<<). Increased permeability across BECs after meth treatment was also observed in vitro through dose-dependent decreases in transendothelial electrical resistance, a method commonly used to measure paracellular permeability (Mahajan et al.,
n2:mentions: n3:21803344

Subject Item: _:vb16821664
rdf:type: n2:Context
rdf:value: permeability across BECs after meth treatment was also observed in vitro through dose-dependent decreases in transendothelial electrical resistance, a method commonly used to measure paracellular permeability (Mahajan et al., >>2008<<; Zhang et al., 2009; Abdul Muneer et al., 2011).
n2:mentions: n3:18329007

Subject Item: _:vb16821665
rdf:type: n2:Context
rdf:value: across BECs after meth treatment was also observed in vitro through dose-dependent decreases in transendothelial electrical resistance, a method commonly used to measure paracellular permeability (Mahajan et al., 2008; Zhang et al., >>2009<<; Abdul Muneer et al., 2011). Clinical studies report increased levels of peripheral toxins, like HIV and hepatitis C virus, in the brain parenchyma of meth-abusing humans (Nath et al., 2001;Letendre et al., 2005, 2007; Schep et al., 2010).
n2:mentions: n3:19374890

Subject Item: _:vb16821666
rdf:type: n2:Context
rdf:value: was also observed in vitro through dose-dependent decreases in transendothelial electrical resistance, a method commonly used to measure paracellular permeability (Mahajan et al., 2008; Zhang et al., 2009; Abdul Muneer et al., >>2011<<). Clinical studies report increased levels of peripheral toxins, like HIV and hepatitis C virus, in the brain parenchyma of meth-abusing humans (Nath et al., 2001;Letendre et al., 2005, 2007; Schep et al., 2010).
n2:mentions: n3:21426580

Subject Item: _:vb16821667
rdf:type: n2:Context
rdf:value: Clinical studies report increased levels of peripheral toxins, like HIV and hepatitis C virus, in the brain parenchyma of meth-abusing humans (Nath et al., >>2001<<;Letendre et al., 2005, 2007; Schep et al., 2010).
n2:mentions: n3:11519485

Subject Item: _:vb16821668
rdf:type: n2:Context
rdf:value: Clinical studies report increased levels of peripheral toxins, like HIV and hepatitis C virus, in the brain parenchyma of meth-abusing humans (Nath et al., 2001;Letendre et al., >>2005<<, 2007; Schep et al., 2010).
n2:mentions: n3:16251831

Subject Item: _:vb16821669
rdf:type: n2:Context
rdf:value: Clinical studies report increased levels of peripheral toxins, like HIV and hepatitis C virus, in the brain parenchyma of meth-abusing humans (Nath et al., 2001;Letendre et al., 2005, >>2007<<; Schep et al., 2010).
n2:mentions: n3:17597450

Subject Item: _:vb16821670
rdf:type: n2:Context
rdf:value: Clinical studies report increased levels of peripheral toxins, like HIV and hepatitis C virus, in the brain parenchyma of meth-abusing humans (Nath et al., 2001;Letendre et al., 2005, 2007; Schep et al., >>2010<<). In fact, 70% of individuals undergoing treatment for hepatitis C in one study were self-reported chronic meth abusers (Letendre et al., 2007). These individuals had a higher hepatitis C viral load in the brain than meth-naïve
n2:mentions: n3:20849327

Subject Item: _:vb16821671
rdf:type: n2:Context
rdf:value: In fact, 70% of individuals undergoing treatment for hepatitis C in one study were self-reported chronic meth abusers (Letendre et al., >>2007<<). These individuals had a higher hepatitis C viral load in the brain than meth-naïve individuals diagnosed with hepatitis C suggesting that meth-induced BBB dysfunction can increase viral penetration into the CNS (Letendre et al., 2007).
n2:mentions: n3:17597450

Subject Item: _:vb16821672
rdf:type: n2:Context
rdf:value: These individuals had a higher hepatitis C viral load in the brain than meth-naïve individuals diagnosed with hepatitis C suggesting that meth-induced BBB dysfunction can increase viral penetration into the CNS (Letendre et al., >>2007<<).
n2:mentions: n3:17597450

Subject Item: _:vb16821673
rdf:type: n2:Context
rdf:value: Meth treatment decreases the expression of ZO-1, occludin, and claudin-5 in both in vivo and in vitro studies (Mahajan et al., >>2008<<; Ramirez et al., 2009; Banerjee et al., 2010; Abdul Muneer et al., 2011; Martins et al., 2011).
n2:mentions: n3:18329007

Subject Item: _:vb16821674
rdf:type: n2:Context
rdf:value: Meth treatment decreases the expression of ZO-1, occludin, and claudin-5 in both in vivo and in vitro studies (Mahajan et al., 2008; Ramirez et al., >>2009<<; Banerjee et al., 2010; Abdul Muneer et al., 2011; Martins et al., 2011).
n2:mentions: n3:19654589

Subject Item: _:vb16821675
rdf:type: n2:Context
rdf:value: Meth treatment decreases the expression of ZO-1, occludin, and claudin-5 in both in vivo and in vitro studies (Mahajan et al., 2008; Ramirez et al., 2009; Banerjee et al., >>2010<<; Abdul Muneer et al., 2011; Martins et al., 2011).
n2:mentions: n3:20188164

Subject Item: _:vb16821676
rdf:type: n2:Context
rdf:value: Meth treatment decreases the expression of ZO-1, occludin, and claudin-5 in both in vivo and in vitro studies (Mahajan et al., 2008; Ramirez et al., 2009; Banerjee et al., 2010; Abdul Muneer et al., >>2011<<; Martins et al., 2011).
n2:mentions: n3:21426580

Subject Item: _:vb16821677
rdf:type: n2:Context
rdf:value: Meth treatment decreases the expression of ZO-1, occludin, and claudin-5 in both in vivo and in vitro studies (Mahajan et al., 2008; Ramirez et al., 2009; Banerjee et al., 2010; Abdul Muneer et al., 2011; Martins et al., >>2011<<). Additionally, meth can also alter other BBB cell types and interactions. For example, meth increases the expression of peptidases, like MMP-1 and MMP-9, which are involved in degrading certain tight junction proteins to produce
n2:mentions: n3:21803344

Subject Item: _:vb16821678
rdf:type: n2:Context
rdf:value: For example, meth increases the expression of peptidases, like MMP-1 and MMP-9, which are involved in degrading certain tight junction proteins to produce structural changes to the BBB basement membrane (Conant et al., >>2004<<). Meth also activates microglia and astrocytes within the neuro(glio)vascular unit which may contribute to meth-induced neurotoxicity, potentially through the secretion of inflammatory cytokines, chemokines, and vasoactive factors
n2:mentions: n3:14982725

Subject Item: _:vb16821679
rdf:type: n2:Context
rdf:value: microglia and astrocytes within the neuro(glio)vascular unit which may contribute to meth-induced neurotoxicity, potentially through the secretion of inflammatory cytokines, chemokines, and vasoactive factors (Kiyatkin et al., >>2007<<; Wisor et al., 2011). These structural and functional changes within the BBB/neuro(glio)vascular unit can also result in brain edema and disruption of proper ion flow across the barrier (Sharma and Kiyatkin, 2009).
n2:mentions: n3:17767502

Subject Item: _:vb16821680
rdf:type: n2:Context
rdf:value: astrocytes within the neuro(glio)vascular unit which may contribute to meth-induced neurotoxicity, potentially through the secretion of inflammatory cytokines, chemokines, and vasoactive factors (Kiyatkin et al., 2007; Wisor et al., >>2011<<). These structural and functional changes within the BBB/neuro(glio)vascular unit can also result in brain edema and disruption of proper ion flow across the barrier (Sharma and Kiyatkin, 2009).
n2:mentions: n3:21333736

Subject Item: _:vb16821681
rdf:type: n2:Context
rdf:value: These structural and functional changes within the BBB/neuro(glio)vascular unit can also result in brain edema and disruption of proper ion flow across the barrier (Sharma and Kiyatkin, >>2009<<).
n2:mentions: n3:18773954

Subject Item: _:vb16821682
rdf:type: n2:Context
rdf:value: A single 30 mg/kg intraperitoneal injection of meth increases the expression TNFα and IL-6 in the hippocampus, frontal cortex, and striatum in mice (Goncalves et al., >>2008<<). Similar increases in TNFα, IL-1β, and IL-6 are reported after multiple meth treatments and are potentially linked to meth-induced microglial activation (Cadet et al., 1994; Lai et al., 2009; Goncalves et al., 2010). Mahajan et al.
n2:mentions: n3:18991854

Subject Item: _:vb16821683
rdf:type: n2:Context
rdf:value: Similar increases in TNFα, IL-1β, and IL-6 are reported after multiple meth treatments and are potentially linked to meth-induced microglial activation (Cadet et al., >>1994<<; Lai et al., 2009; Goncalves et al., 2010).
n2:mentions: n3:7505315

Subject Item: _:vb16821684
rdf:type: n2:Context
rdf:value: Similar increases in TNFα, IL-1β, and IL-6 are reported after multiple meth treatments and are potentially linked to meth-induced microglial activation (Cadet et al., 1994; Lai et al., >>2009<<; Goncalves et al., 2010).
n2:mentions: n3:19271121

Subject Item: _:vb16821685
rdf:type: n2:Context
rdf:value: Similar increases in TNFα, IL-1β, and IL-6 are reported after multiple meth treatments and are potentially linked to meth-induced microglial activation (Cadet et al., 1994; Lai et al., 2009; Goncalves et al., >>2010<<). Mahajan et al. (2008) showed that exposure to 50 nM meth produced a 47% increase in the transmigration of peripheral blood mononuclear cells using an in vitro BBB model. Meth-induced increases in glial activation as well as TNFα and TNF
n2:mentions: n3:20074221

Subject Item: _:vb16821686
rdf:type: n2:Context
rdf:value: Mahajan et al. (>>2008<<) showed that exposure to 50 nM meth produced a 47% increase in the transmigration of peripheral blood mononuclear cells using an in vitro BBB model.
n2:mentions: n3:18329007

Subject Item: _:vb16821687
rdf:type: n2:Context
rdf:value: glial activation as well as TNFα and TNF receptor expression were attenuated with pre-treatment of indomethacin, an anti-inflammatory agent, suggesting a potential therapeutic target for impeding meth-neurotoxicity (Goncalves et al., >>2010<<). In summary, neuroinflammation contributes to the neurotoxicities seen after meth exposure and potentiates the feed-forward cycle between neuroinflammation and BBB damage to produce prolonged BBB damage (see Table 1 for a summary of the
n2:mentions: n3:20074221

Subject Item: _:vb16821688
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (>>2008<<); 2Zhang et al. (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer
n2:mentions: n3:18329007

Subject Item: _:vb16821689
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (2008); 2Zhang et al. (>>2009<<); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008);
n2:mentions: n3:19374890

Subject Item: _:vb16821690
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (2008); 2Zhang et al. (2009); 3Abdul Muneer et al. (>>2011<<); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin
n2:mentions: n3:21426580

Subject Item: _:vb16821691
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (2008); 2Zhang et al. (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (>>2009<<); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007);
n2:mentions: n3:19654589

Subject Item: _:vb16821692
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (2008); 2Zhang et al. (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (>>2004<<); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath
n2:mentions: n3:14982725

Subject Item: _:vb16821693
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (2008); 2Zhang et al. (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (>>2011<<); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001);
n2:mentions: n3:21979424

Subject Item: _:vb16821694
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (2008); 2Zhang et al. (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (>>2011<<); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (2005, 2007).
n2:mentions: n3:21803344

Subject Item: _:vb16821695
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (2008); 2Zhang et al. (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (>>2009<<); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (2005, 2007).
n2:mentions: n3:18773954

Subject Item: _:vb16821696
rdf:type: n2:Context
rdf:value: 1Mahajan et al. (2008); 2Zhang et al. (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (>>2011<<); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (2005, 2007).
n2:mentions: n3:20931246

Subject Item: _:vb16821697
rdf:type: n2:Context
rdf:value: al. (2008); 2Zhang et al. (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (>>2006<<); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (2005, 2007).
n2:mentions: n3:17105918

Subject Item: _:vb16821698
rdf:type: n2:Context
rdf:value: (2009); 3Abdul Muneer et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (>>2008<<); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (2005, 2007).
n2:mentions: n3:18991857

Subject Item: _:vb16821699
rdf:type: n2:Context
rdf:value: et al. (2011); 4Ramirez et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (>>2010<<); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (2005, 2007).
n2:mentions: n3:19890265

Subject Item: _:vb16821700
rdf:type: n2:Context
rdf:value: et al. (2009); 5Conant et al. (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (>>2007<<); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (2005, 2007).
n2:mentions: n3:17767502

Subject Item: _:vb16821701
rdf:type: n2:Context
rdf:value: (2004); 6Kousik et al. (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (>>2010<<); 15Nath et al. (2001); 16Letendre et al. (2005, 2007).
n2:mentions: n3:20188164

Subject Item: _:vb16821702
rdf:type: n2:Context
rdf:value: (2011); 7Martins et al. (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (>>2001<<); 16Letendre et al. (2005, 2007).
n2:mentions: n3:11519485

Subject Item: _:vb16821703
rdf:type: n2:Context
rdf:value: (2011); 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (>>2005<<, 2007).
n2:mentions: n3:16251831

Subject Item: _:vb16821704
rdf:type: n2:Context
rdf:value: 8Sharma and Kiyatkin (2009); 9Kiyatkin and Sharma (2011); 10Sharma and Ali (2006); 11Bowyer et al. (2008); 12Kuroda et al. (2010); 13Kiyatkin et al. (2007); 14Banerjee et al. (2010); 15Nath et al. (2001); 16Letendre et al. (2005, >>2007<<).
n2:mentions: n3:17597450

Subject Item: _:vb16821705
rdf:type: n2:Context
rdf:value: Like other amphetamines, MDMA increases the release of monoamines from nerve terminals through interactions with the serotonin transporter (SERT) and dopamine transporter (DAT; Sulzer et al., >>2005<<). MDMA has a higher affinity for SERT than DAT resulting in a greater release of 5-HT than DA (Rothman and Baumann, 2003). Like meth, secondary release of glutamate may contribute to the neurotoxic effects of MDMA (Nash and Yamamoto,
n2:mentions: n3:15955613

Subject Item: _:vb16821706
rdf:type: n2:Context
rdf:value: MDMA has a higher affinity for SERT than DAT resulting in a greater release of 5-HT than DA (Rothman and Baumann, >>2003<<). Like meth, secondary release of glutamate may contribute to the neurotoxic effects of MDMA (Nash and Yamamoto, 1992). Though acute consequences of MDMA use have been well-studied, long-term effects and potential neurotoxicities are not
n2:mentions: n3:14612135

Subject Item: _:vb16821707
rdf:type: n2:Context
rdf:value: Like meth, secondary release of glutamate may contribute to the neurotoxic effects of MDMA (Nash and Yamamoto, >>1992<<). Though acute consequences of MDMA use have been well-studied, long-term effects and potential neurotoxicities are not well known. MDMA appears to be selectively toxic to 5-HT terminals and produces long-lasting depletions of 5-HT in the
n2:mentions: n3:1356579

Subject Item: _:vb16821708
rdf:type: n2:Context
rdf:value: MDMA appears to be selectively toxic to 5-HT terminals and produces long-lasting depletions of 5-HT in the hippocampus, prefrontal cortex, amygdala, and striatum (Morgan and Gibb, >>1980<<; Ricaurte et al., 1985, 1988).
n2:mentions: n3:6106905

Subject Item: _:vb16821709
rdf:type: n2:Context
rdf:value: MDMA appears to be selectively toxic to 5-HT terminals and produces long-lasting depletions of 5-HT in the hippocampus, prefrontal cortex, amygdala, and striatum (Morgan and Gibb, 1980; Ricaurte et al., >>1985<<, 1988). Moreover, thioester metabolites of MDMA, including 3,4-dihydroxyamphetamine (DHA), also produce long-term depletion of 5-HT (Monks et al., 2004). Though 5-HT toxicities have been identified in multiple brain areas, the mechanisms
n2:mentions: n3:4023719

Subject Item: _:vb16821710
rdf:type: n2:Context
rdf:value: MDMA appears to be selectively toxic to 5-HT terminals and produces long-lasting depletions of 5-HT in the hippocampus, prefrontal cortex, amygdala, and striatum (Morgan and Gibb, 1980; Ricaurte et al., 1985, >>1988<<). Moreover, thioester metabolites of MDMA, including 3,4-dihydroxyamphetamine (DHA), also produce long-term depletion of 5-HT (Monks et al., 2004). Though 5-HT toxicities have been identified in multiple brain areas, the mechanisms
n2:mentions: n3:2454332

Subject Item: _:vb16821711
rdf:type: n2:Context
rdf:value: Moreover, thioester metabolites of MDMA, including 3,4-dihydroxyamphetamine (DHA), also produce long-term depletion of 5-HT (Monks et al., >>2004<<). Though 5-HT toxicities have been identified in multiple brain areas, the mechanisms underlying this selective toxicity remain unknown.
n2:mentions: n3:15228153

Subject Item: _:vb16821712
rdf:type: n2:Context
rdf:value: Increased leakage of Evans Blue or trypan blue as well as increased IgG immunostaining were reported in several cortical areas, hippocampus, cerebellum, and striatum of rats treated acutely with MDMA (Yamamoto and Bankson, >>2005<<; Sharma and Ali, 2008; Torres et al., 2011). BBB dysfunction was observed immediately following acute MDMA treatment and up to 10 weeks following an acute injection.
n2:mentions: n3:16808729

Subject Item: _:vb16821713
rdf:type: n2:Context
rdf:value: leakage of Evans Blue or trypan blue as well as increased IgG immunostaining were reported in several cortical areas, hippocampus, cerebellum, and striatum of rats treated acutely with MDMA (Yamamoto and Bankson, 2005; Sharma and Ali, >>2008<<; Torres et al., 2011). BBB dysfunction was observed immediately following acute MDMA treatment and up to 10 weeks following an acute injection.
n2:mentions: n3:18991870

Subject Item: _:vb16821714
rdf:type: n2:Context
rdf:value: or trypan blue as well as increased IgG immunostaining were reported in several cortical areas, hippocampus, cerebellum, and striatum of rats treated acutely with MDMA (Yamamoto and Bankson, 2005; Sharma and Ali, 2008; Torres et al., >>2011<<). BBB dysfunction was observed immediately following acute MDMA treatment and up to 10 weeks following an acute injection.
n2:mentions: n3:21595923

Subject Item: _:vb16821715
rdf:type: n2:Context
rdf:value: Increased BBB permeability after MDMA treatment was associated with increased parenchymal penetration of endogenous albumin (Sharma and Ali, >>2008<<), increased activation of astrocytes, and microglia (Monks et al., 2004), and increased brain water content suggesting edema (Sharma and Ali, 2008).
n2:mentions: n3:18991870

Subject Item: _:vb16821716
rdf:type: n2:Context
rdf:value: Increased BBB permeability after MDMA treatment was associated with increased parenchymal penetration of endogenous albumin (Sharma and Ali, 2008), increased activation of astrocytes, and microglia (Monks et al., >>2004<<), and increased brain water content suggesting edema (Sharma and Ali, 2008).
n2:mentions: n3:15228153

Subject Item: _:vb16821717
rdf:type: n2:Context
rdf:value: with increased parenchymal penetration of endogenous albumin (Sharma and Ali, 2008), increased activation of astrocytes, and microglia (Monks et al., 2004), and increased brain water content suggesting edema (Sharma and Ali, >>2008<<).
n2:mentions: n3:18991870

Subject Item: _:vb16821718
rdf:type: n2:Context
rdf:value: In addition to altering BBB permeability, MDMA increases expression of pro-inflammatory cytokines, including IL-1β, in brain tissue (Torres et al., >>2011<<). These cytokines can contribute to the feed-forward cycle between BBB dysfunction and neuroinflammation.
n2:mentions: n3:21595923

Subject Item: _:vb16821719
rdf:type: n2:Context
rdf:value: MDMA abuse also leads to oxidative stress (Yamamoto and Bankson, >>2005<<). MDMA-induced excess release of DA and 5-HT results in the formation of ROS, DAQ, and toxic metabolites from 5-HT oxidation (Quinton and Yamamoto, 2006).
n2:mentions: n3:16808729

Subject Item: _:vb16821720
rdf:type: n2:Context
rdf:value: MDMA-induced excess release of DA and 5-HT results in the formation of ROS, DAQ, and toxic metabolites from 5-HT oxidation (Quinton and Yamamoto, >>2006<<). The accumulation of toxic free radicals increases the susceptibility of brain tissue to ischemic injury and triggers a variety of signaling cascades leading to BBB dysfunction, brain edema, and neuroinflammation (Gu et al., 2012). It is
n2:mentions: n3:16796384

Subject Item: _:vb16821721
rdf:type: n2:Context
rdf:value: The accumulation of toxic free radicals increases the susceptibility of brain tissue to ischemic injury and triggers a variety of signaling cascades leading to BBB dysfunction, brain edema, and neuroinflammation (Gu et al., >>2012<<). It is likely that the oxidative stress and neuroinflammation produced by MDMA results in BBB dysfunction, though further research is needed to verify if MDMA has a direct detrimental effect on the BBB (see Table 2 for a summary of the
n2:mentions: n3:22007835

Subject Item: _:vb16821722
rdf:type: n2:Context
rdf:value: 1Sharma and Ali (>>2008<<); 2Torres et al. (2011); 3Monks et al. (2004); 4Orio et al. (2004); 5O’Shea et al. (2005); 6Yamamoto and Bankson (2005); 7Yamamoto and Raudensky (2008).
n2:mentions: n3:18991870

Subject Item: _:vb16821723
rdf:type: n2:Context
rdf:value: 1Sharma and Ali (2008); 2Torres et al. (>>2011<<); 3Monks et al. (2004); 4Orio et al. (2004); 5O’Shea et al. (2005); 6Yamamoto and Bankson (2005); 7Yamamoto and Raudensky (2008).
n2:mentions: n3:21595923

Subject Item: _:vb16821724
rdf:type: n2:Context
rdf:value: 1Sharma and Ali (2008); 2Torres et al. (2011); 3Monks et al. (>>2004<<); 4Orio et al. (2004); 5O’Shea et al. (2005); 6Yamamoto and Bankson (2005); 7Yamamoto and Raudensky (2008).
n2:mentions: n3:15228153

Subject Item: _:vb16821725
rdf:type: n2:Context
rdf:value: 1Sharma and Ali (2008); 2Torres et al. (2011); 3Monks et al. (2004); 4Orio et al. (>>2004<<); 5O’Shea et al. (2005); 6Yamamoto and Bankson (2005); 7Yamamoto and Raudensky (2008).
n2:mentions: n3:15189347

Subject Item: _:vb16821726
rdf:type: n2:Context
rdf:value: 1Sharma and Ali (2008); 2Torres et al. (2011); 3Monks et al. (2004); 4Orio et al. (2004); 5O’Shea et al. (>>2005<<); 6Yamamoto and Bankson (2005); 7Yamamoto and Raudensky (2008).
n2:mentions: n3:16165281

Subject Item: _:vb16821727
rdf:type: n2:Context
rdf:value: 1Sharma and Ali (2008); 2Torres et al. (2011); 3Monks et al. (2004); 4Orio et al. (2004); 5O’Shea et al. (2005); 6Yamamoto and Bankson (>>2005<<); 7Yamamoto and Raudensky (2008).
n2:mentions: n3:16808729

Subject Item: _:vb16821728
rdf:type: n2:Context
rdf:value: 1Sharma and Ali (2008); 2Torres et al. (2011); 3Monks et al. (2004); 4Orio et al. (2004); 5O’Shea et al. (2005); 6Yamamoto and Bankson (2005); 7Yamamoto and Raudensky (>>2008<<).
n2:mentions: n3:18709468

Subject Item: _:vb16821729
rdf:type: n2:Context
rdf:value: Cocaine inhibits monoamine reuptake, particularly through binding DAT (Barnett et al., >>1981<<). While cocaine abuse was at its highest levels in the 1970–1980s, the United States is still the world’s number one importer and user with approximately 1.9 million current cocaine abusers (NSDUH 2008).
n2:mentions: n3:7242115

Subject Item: _:vb16821730
rdf:type: n2:Context
rdf:value: Cocaine abuse is not linked to DA or 5-HT terminal damage (Bennett et al., >>1993<<) though cocaine can produce oxidative stress and neuroinflammation.
n2:mentions: n3:8095976

Subject Item: _:vb16821731
rdf:type: n2:Context
rdf:value: Chronic cocaine administration (30 mg/kg/day intraperitoneal injection) ruptures the neurovascular capillaries and basement membranes of rats (Barroso-Moguel et al., >>1997<<). Increased BBB permeability marked by approximately 50% more Evans Blue or sodium fluorescein leakage from blood to brain after cocaine exposure has also been observed in rodents (Sharma et al., 2009; Yang et al., 2010; Yao et al., 2011).
n2:mentions: n3:9242352

Subject Item: _:vb16821732
rdf:type: n2:Context
rdf:value: Increased BBB permeability marked by approximately 50% more Evans Blue or sodium fluorescein leakage from blood to brain after cocaine exposure has also been observed in rodents (Sharma et al., >>2009<<; Yang et al., 2010; Yao et al., 2011).
n2:mentions: n3:19897082

Subject Item: _:vb16821733
rdf:type: n2:Context
rdf:value: Increased BBB permeability marked by approximately 50% more Evans Blue or sodium fluorescein leakage from blood to brain after cocaine exposure has also been observed in rodents (Sharma et al., 2009; Yang et al., >>2010<<; Yao et al., 2011).
n2:mentions: n3:20976166

Subject Item: _:vb16821734
rdf:type: n2:Context
rdf:value: Increased BBB permeability marked by approximately 50% more Evans Blue or sodium fluorescein leakage from blood to brain after cocaine exposure has also been observed in rodents (Sharma et al., 2009; Yang et al., 2010; Yao et al., >>2011<<). Whole animal studies are more recent in this field as most studies investigating the effects of cocaine on BBB integrity use an in vitro BBB model comprised of brain microvascular endothelial cells and C6 astrocytes.
n2:mentions: n3:21508219

Subject Item: _:vb16821735
rdf:type: n2:Context
rdf:value: Decreases in transendothelial electrical resistance and increases in FITC-Dextran leakage across an endothelial monolayer indicates increased permeability across BECs after cocaine treatment (Fiala et al., >>1998<<, 2005; Zhang et al., 1998; Gandhi et al., 2010; Yao et al., 2011).
n2:mentions: n3:9666272

Subject Item: _:vb16821736
rdf:type: n2:Context
rdf:value: Decreases in transendothelial electrical resistance and increases in FITC-Dextran leakage across an endothelial monolayer indicates increased permeability across BECs after cocaine treatment (Fiala et al., 1998, >>2005<<; Zhang et al., 1998; Gandhi et al., 2010; Yao et al., 2011).
n2:mentions: n3:16036808

Subject Item: _:vb16821737
rdf:type: n2:Context
rdf:value: Decreases in transendothelial electrical resistance and increases in FITC-Dextran leakage across an endothelial monolayer indicates increased permeability across BECs after cocaine treatment (Fiala et al., 1998, 2005; Zhang et al., >>1998<<; Gandhi et al., 2010; Yao et al., 2011). Clinical studies reveal similar BBB breakdown in the basal ganglia and increased HIV penetration into the CNS of cocaine-abusing humans (Nath et al., 2001).
n2:mentions: n3:10065903

Subject Item: _:vb16821738
rdf:type: n2:Context
rdf:value: electrical resistance and increases in FITC-Dextran leakage across an endothelial monolayer indicates increased permeability across BECs after cocaine treatment (Fiala et al., 1998, 2005; Zhang et al., 1998; Gandhi et al., >>2010<<; Yao et al., 2011). Clinical studies reveal similar BBB breakdown in the basal ganglia and increased HIV penetration into the CNS of cocaine-abusing humans (Nath et al., 2001).
n2:mentions: n3:20624003

Subject Item: _:vb16821739
rdf:type: n2:Context
rdf:value: resistance and increases in FITC-Dextran leakage across an endothelial monolayer indicates increased permeability across BECs after cocaine treatment (Fiala et al., 1998, 2005; Zhang et al., 1998; Gandhi et al., 2010; Yao et al., >>2011<<). Clinical studies reveal similar BBB breakdown in the basal ganglia and increased HIV penetration into the CNS of cocaine-abusing humans (Nath et al., 2001).
n2:mentions: n3:21508219

Subject Item: _:vb16821740
rdf:type: n2:Context
rdf:value: Clinical studies reveal similar BBB breakdown in the basal ganglia and increased HIV penetration into the CNS of cocaine-abusing humans (Nath et al., >>2001<<).
n2:mentions: n3:11519485

Subject Item: _:vb16821741
rdf:type: n2:Context
rdf:value: Cocaine-induced BBB dysfunction is partially characterized by loss of, or alterations in, tight junction protein complexes (Fiala et al., >>2005<<, 2008). Significant decreases in ZO-1 and JAM-2 occur in both rodents and in vitro BBB preparations (Dhillon et al., 2008; Gandhi et al., 2010; Yao et al., 2011).
n2:mentions: n3:16036808

Subject Item: _:vb16821742
rdf:type: n2:Context
rdf:value: Cocaine-induced BBB dysfunction is partially characterized by loss of, or alterations in, tight junction protein complexes (Fiala et al., 2005, >>2008<<). Significant decreases in ZO-1 and JAM-2 occur in both rodents and in vitro BBB preparations (Dhillon et al., 2008; Gandhi et al., 2010; Yao et al., 2011).
n2:mentions: n3:19440461

Subject Item: _:vb16821743
rdf:type: n2:Context
rdf:value: Significant decreases in ZO-1 and JAM-2 occur in both rodents and in vitro BBB preparations (Dhillon et al., >>2008<<; Gandhi et al., 2010; Yao et al., 2011).
n2:mentions: n3:18046654

Subject Item: _:vb16821744
rdf:type: n2:Context
rdf:value: Significant decreases in ZO-1 and JAM-2 occur in both rodents and in vitro BBB preparations (Dhillon et al., 2008; Gandhi et al., >>2010<<; Yao et al., 2011).
n2:mentions: n3:20624003

Subject Item: _:vb16821745
rdf:type: n2:Context
rdf:value: Significant decreases in ZO-1 and JAM-2 occur in both rodents and in vitro BBB preparations (Dhillon et al., 2008; Gandhi et al., 2010; Yao et al., >>2011<<). Cocaine treatment also increases gene expression of factors, including MMP-1, that contribute to basement membrane actin rearrangement resulting in stress fiber formation around cerebral vessels (Nair et al., 2004; Fiala et al., 2005;
n2:mentions: n3:21508219

Subject Item: _:vb16821746
rdf:type: n2:Context
rdf:value: Cocaine treatment also increases gene expression of factors, including MMP-1, that contribute to basement membrane actin rearrangement resulting in stress fiber formation around cerebral vessels (Nair et al., >>2004<<; Fiala et al., 2005; Dhillon et al., 2008).
n2:mentions: n3:15579280

Subject Item: _:vb16821747
rdf:type: n2:Context
rdf:value: Cocaine treatment also increases gene expression of factors, including MMP-1, that contribute to basement membrane actin rearrangement resulting in stress fiber formation around cerebral vessels (Nair et al., 2004; Fiala et al., >>2005<<; Dhillon et al., 2008).
n2:mentions: n3:16036808

Subject Item: _:vb16821748
rdf:type: n2:Context
rdf:value: also increases gene expression of factors, including MMP-1, that contribute to basement membrane actin rearrangement resulting in stress fiber formation around cerebral vessels (Nair et al., 2004; Fiala et al., 2005; Dhillon et al., >>2008<<). Persistent loss of, or conformation changes in tight junction proteins, and reorganization of basement membrane fibers leave the brain open to peripheral toxin penetration leading to CNS disorders linked with cocaine abuse (see Table 3
n2:mentions: n3:18046654

Subject Item: _:vb16821749
rdf:type: n2:Context
rdf:value: 1Fiala et al. (>>2005<<); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al.
n2:mentions: n3:16036808

Subject Item: _:vb16821750
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (>>2010<<); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et
n2:mentions: n3:20624003

Subject Item: _:vb16821751
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (>>1998<<); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma
n2:mentions: n3:10065903

Subject Item: _:vb16821752
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (>>1998<<); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang
n2:mentions: n3:9666272

Subject Item: _:vb16821753
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (>>2011<<); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000);
n2:mentions: n3:21508219

Subject Item: _:vb16821754
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (>>1996<<); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001);
n2:mentions: n3:8787655

Subject Item: _:vb16821755
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (>>2008<<); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:19440461

Subject Item: _:vb16821756
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (>>2008<<); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:18046654

Subject Item: _:vb16821757
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (>>2004<<); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:15579280

Subject Item: _:vb16821758
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (>>1999<<); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:10219256

Subject Item: _:vb16821759
rdf:type: n2:Context
rdf:value: 1Fiala et al. (2005); 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (>>2001<<); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:11716818

Subject Item: _:vb16821760
rdf:type: n2:Context
rdf:value: 2Gandhi et al. (2010); 3Zhang et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (>>2011<<); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:21508219

Subject Item: _:vb16821761
rdf:type: n2:Context
rdf:value: et al. (1998); 4Fiala et al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (>>1997<<); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:9242352

Subject Item: _:vb16821762
rdf:type: n2:Context
rdf:value: al. (1998); 5Yao et al. (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (>>2009<<); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:19897082

Subject Item: _:vb16821763
rdf:type: n2:Context
rdf:value: (2011); 6Fiala et al. (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (>>2000<<); 16Nath et al. (2001); 17Buch et al. (2011).
n2:mentions: n3:10864098

Subject Item: _:vb16821764
rdf:type: n2:Context
rdf:value: (1996); 7Fiala et al. (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (>>2001<<); 17Buch et al. (2011).
n2:mentions: n3:11519485

Subject Item: _:vb16821765
rdf:type: n2:Context
rdf:value: (2008); 8Dhillon et al. (2008); 9Nair et al. (2004); 10Gan et al. (1999); 11Lee et al. (2001); 12Yao et al. (2011); 13Barroso-Moguel et al. (1997); 14Sharma et al. (2009); 15Chang et al. (2000); 16Nath et al. (2001); 17Buch et al. (>>2011<<).
n2:mentions: n3:21766222

Subject Item: _:vb16821766
rdf:type: n2:Context
rdf:value: vascular cell adhesion molecule 1 (VCAM-1), endothelial-leukocyte adhesion molecule (ELAM or selectin-1), and platelet endothelial cell adhesion molecule 1 (PECAM1), have been indentified in both preclinical studies (Fiala et al., >>1998<<, 2005; Gan et al., 1999; Chang et al., 2000) and in cocaine-abusing humans (Buch et al., 2011).
n2:mentions: n3:9666272

Subject Item: _:vb16821767
rdf:type: n2:Context
rdf:value: cell adhesion molecule 1 (VCAM-1), endothelial-leukocyte adhesion molecule (ELAM or selectin-1), and platelet endothelial cell adhesion molecule 1 (PECAM1), have been indentified in both preclinical studies (Fiala et al., 1998, >>2005<<; Gan et al., 1999; Chang et al., 2000) and in cocaine-abusing humans (Buch et al., 2011).
n2:mentions: n3:16036808

Subject Item: _:vb16821768
rdf:type: n2:Context
rdf:value: molecule 1 (VCAM-1), endothelial-leukocyte adhesion molecule (ELAM or selectin-1), and platelet endothelial cell adhesion molecule 1 (PECAM1), have been indentified in both preclinical studies (Fiala et al., 1998, 2005; Gan et al., >>1999<<; Chang et al., 2000) and in cocaine-abusing humans (Buch et al., 2011).
n2:mentions: n3:10219256

Subject Item: _:vb16821769
rdf:type: n2:Context
rdf:value: endothelial-leukocyte adhesion molecule (ELAM or selectin-1), and platelet endothelial cell adhesion molecule 1 (PECAM1), have been indentified in both preclinical studies (Fiala et al., 1998, 2005; Gan et al., 1999; Chang et al., >>2000<<) and in cocaine-abusing humans (Buch et al., 2011).
n2:mentions: n3:10864098

Subject Item: _:vb16821770
rdf:type: n2:Context
rdf:value: or selectin-1), and platelet endothelial cell adhesion molecule 1 (PECAM1), have been indentified in both preclinical studies (Fiala et al., 1998, 2005; Gan et al., 1999; Chang et al., 2000) and in cocaine-abusing humans (Buch et al., >>2011<<). Increases in circulating leukocytes and cell adhesion molecules on leukocytes have also been reported with cocaine treatment in rodents and in vitro (Chang et al., 2000; Nair et al., 2004).
n2:mentions: n3:21766222

Subject Item: _:vb16821771
rdf:type: n2:Context
rdf:value: Increases in circulating leukocytes and cell adhesion molecules on leukocytes have also been reported with cocaine treatment in rodents and in vitro (Chang et al., >>2000<<; Nair et al., 2004).
n2:mentions: n3:10864098

Subject Item: _:vb16821772
rdf:type: n2:Context
rdf:value: Increases in circulating leukocytes and cell adhesion molecules on leukocytes have also been reported with cocaine treatment in rodents and in vitro (Chang et al., 2000; Nair et al., >>2004<<). Increases in cell adhesion molecules on the BBB endothelium and on leukocytes promote more leukocyte extravasation from blood to brain (Barroso-Moguel et al., 1997; Gan et al., 1999). Indeed, cocaine treatment in vitro results in a 100%
n2:mentions: n3:15579280

Subject Item: _:vb16821773
rdf:type: n2:Context
rdf:value: Increases in cell adhesion molecules on the BBB endothelium and on leukocytes promote more leukocyte extravasation from blood to brain (Barroso-Moguel et al., >>1997<<; Gan et al., 1999).
n2:mentions: n3:9242352

Subject Item: _:vb16821774
rdf:type: n2:Context
rdf:value: Increases in cell adhesion molecules on the BBB endothelium and on leukocytes promote more leukocyte extravasation from blood to brain (Barroso-Moguel et al., 1997; Gan et al., >>1999<<). Indeed, cocaine treatment in vitro results in a 100% increase in the number of peripheral blood mononuclear cells migrating across BECs (Fiala et al., 1998, 2008; Zhang et al., 1998). Cocaine-induced increases in leukocyte-endothelial
n2:mentions: n3:10219256

Subject Item: _:vb16821775
rdf:type: n2:Context
rdf:value: Indeed, cocaine treatment in vitro results in a 100% increase in the number of peripheral blood mononuclear cells migrating across BECs (Fiala et al., >>1998<<, 2008; Zhang et al., 1998).
n2:mentions: n3:9666272

Subject Item: _:vb16821776
rdf:type: n2:Context
rdf:value: Indeed, cocaine treatment in vitro results in a 100% increase in the number of peripheral blood mononuclear cells migrating across BECs (Fiala et al., 1998, >>2008<<; Zhang et al., 1998).
n2:mentions: n3:19440461

Subject Item: _:vb16821777
rdf:type: n2:Context
rdf:value: Indeed, cocaine treatment in vitro results in a 100% increase in the number of peripheral blood mononuclear cells migrating across BECs (Fiala et al., 1998, 2008; Zhang et al., >>1998<<). Cocaine-induced increases in leukocyte-endothelial adhesion are accompanied by elevated levels of pro-inflammatory cytokines and chemokines. Western blotting and immunostaining reveal increases in the expression of TNFα, IL-6, IL-8,
n2:mentions: n3:10065903

Subject Item: _:vb16821778
rdf:type: n2:Context
rdf:value: Western blotting and immunostaining reveal increases in the expression of TNFα, IL-6, IL-8, nuclear factor kappa B (NFκB), activator protein 1 (AP-1), and CCR2 (Zhang et al., >>1998<<; Gan et al., 1999; Lee et al., 2001; Dhillon et al., 2008).
n2:mentions: n3:10065903

Subject Item: _:vb16821779
rdf:type: n2:Context
rdf:value: Western blotting and immunostaining reveal increases in the expression of TNFα, IL-6, IL-8, nuclear factor kappa B (NFκB), activator protein 1 (AP-1), and CCR2 (Zhang et al., 1998; Gan et al., >>1999<<; Lee et al., 2001; Dhillon et al., 2008).
n2:mentions: n3:10219256

Subject Item: _:vb16821780
rdf:type: n2:Context
rdf:value: Western blotting and immunostaining reveal increases in the expression of TNFα, IL-6, IL-8, nuclear factor kappa B (NFκB), activator protein 1 (AP-1), and CCR2 (Zhang et al., 1998; Gan et al., 1999; Lee et al., >>2001<<; Dhillon et al., 2008).
n2:mentions: n3:11716818

Subject Item: _:vb16821781
rdf:type: n2:Context
rdf:value: Western blotting and immunostaining reveal increases in the expression of TNFα, IL-6, IL-8, nuclear factor kappa B (NFκB), activator protein 1 (AP-1), and CCR2 (Zhang et al., 1998; Gan et al., 1999; Lee et al., 2001; Dhillon et al., >>2008<<). These inflammatory signals are also associated with increased viral invasion of macrophage-tropic HIV across an in vitro BBB (Fiala et al., 1996; Zhang et al., 1998) which may explain the greater neuropathology observed in patients
n2:mentions: n3:18046654

Subject Item: _:vb16821782
rdf:type: n2:Context
rdf:value: These inflammatory signals are also associated with increased viral invasion of macrophage-tropic HIV across an in vitro BBB (Fiala et al., >>1996<<; Zhang et al., 1998) which may explain the greater neuropathology observed in patients co-morbid for HIV infection and cocaine abuse (Fiala et al., 2008).
n2:mentions: n3:8787655

Subject Item: _:vb16821783
rdf:type: n2:Context
rdf:value: These inflammatory signals are also associated with increased viral invasion of macrophage-tropic HIV across an in vitro BBB (Fiala et al., 1996; Zhang et al., >>1998<<) which may explain the greater neuropathology observed in patients co-morbid for HIV infection and cocaine abuse (Fiala et al., 2008).
n2:mentions: n3:10065903

Subject Item: _:vb16821784
rdf:type: n2:Context
rdf:value: viral invasion of macrophage-tropic HIV across an in vitro BBB (Fiala et al., 1996; Zhang et al., 1998) which may explain the greater neuropathology observed in patients co-morbid for HIV infection and cocaine abuse (Fiala et al., >>2008<<). The effects of cocaine on the BBB are likely exacerbated by cocaine-induced neuroinflammation.
n2:mentions: n3:19440461

Subject Item: _:vb16821785
rdf:type: n2:Context
rdf:value: An average cigarette yields approximately 1 mg of absorbed nicotine, a stimulant alkaloid responsible for the addictive-properties of cigarette smoking (Connolly et al., >>2007<<). Nicotine is a soluble small molecule that rapidly diffuses through the BBB and can interact directly with nicotinic acetylcholine receptors (nAChRs) on BECs (Le, 2003). Preclinical studies using rodent models of acute and chronic
n2:mentions: n3:17897974

Subject Item: _:vb16821786
rdf:type: n2:Context
rdf:value: Nicotine is a soluble small molecule that rapidly diffuses through the BBB and can interact directly with nicotinic acetylcholine receptors (nAChRs) on BECs (Le, >>2003<<). Preclinical studies using rodent models of acute and chronic nicotine exposure reported compromised BBB integrity, marked by Evans blue or [14C] sucrose leakage into brain parenchyma. This BBB disruption occurred as early as 2 h after
n2:mentions: n3:12971663

Subject Item: _:vb16821787
rdf:type: n2:Context
rdf:value: This BBB disruption occurred as early as 2 h after acute nicotine and after 6 weeks of chronic exposure (Lin et al., >>1992<<; Uzum et al., 1999; Venisnik, 2000;Hawkins et al., 2004, 2005).
n2:mentions: n3:1420090

Subject Item: _:vb16821788
rdf:type: n2:Context
rdf:value: This BBB disruption occurred as early as 2 h after acute nicotine and after 6 weeks of chronic exposure (Lin et al., 1992; Uzum et al., >>1999<<; Venisnik, 2000;Hawkins et al., 2004, 2005).
n2:mentions: n3:10479471

Subject Item: _:vb16821789
rdf:type: n2:Context
rdf:value: This BBB disruption occurred as early as 2 h after acute nicotine and after 6 weeks of chronic exposure (Lin et al., 1992; Uzum et al., 1999; Venisnik, 2000;Hawkins et al., >>2004<<, 2005). In vitro studies using either brain microvascular endothelial cells alone or in combination with C6 astrocytes revealed increases of FITC-Dextran and [14C]sucrose leakage across the cells after nicotine treatment (Schilling et al.
n2:mentions: n3:15494156

Subject Item: _:vb16821790
rdf:type: n2:Context
rdf:value: This BBB disruption occurred as early as 2 h after acute nicotine and after 6 weeks of chronic exposure (Lin et al., 1992; Uzum et al., 1999; Venisnik, 2000;Hawkins et al., 2004, >>2005<<). In vitro studies using either brain microvascular endothelial cells alone or in combination with C6 astrocytes revealed increases of FITC-Dextran and [14C]sucrose leakage across the cells after nicotine treatment (Schilling et al.,
n2:mentions: n3:15708958

Subject Item: _:vb16821791
rdf:type: n2:Context
rdf:value: In vitro studies using either brain microvascular endothelial cells alone or in combination with C6 astrocytes revealed increases of FITC-Dextran and [14C]sucrose leakage across the cells after nicotine treatment (Schilling et al., >>1992<<; Abbruscato et al., 2002). Nicotine also decreases transendothelial electrical resistance in an in vitro BBB model (Hutamekalin et al., 2008; Rodriguez-Gaztelumendi et al., 2011).
n2:mentions: n3:1521035

Subject Item: _:vb16821792
rdf:type: n2:Context
rdf:value: either brain microvascular endothelial cells alone or in combination with C6 astrocytes revealed increases of FITC-Dextran and [14C]sucrose leakage across the cells after nicotine treatment (Schilling et al., 1992; Abbruscato et al., >>2002<<). Nicotine also decreases transendothelial electrical resistance in an in vitro BBB model (Hutamekalin et al., 2008; Rodriguez-Gaztelumendi et al., 2011).
n2:mentions: n3:12434396

Subject Item: _:vb16821793
rdf:type: n2:Context
rdf:value: Nicotine also decreases transendothelial electrical resistance in an in vitro BBB model (Hutamekalin et al., >>2008<<; Rodriguez-Gaztelumendi et al., 2011).
n2:mentions: n3:17920942

Subject Item: _:vb16821794
rdf:type: n2:Context
rdf:value: Nicotine also decreases transendothelial electrical resistance in an in vitro BBB model (Hutamekalin et al., 2008; Rodriguez-Gaztelumendi et al., >>2011<<). This decrease in resistance is dose-dependent (0.1–100 μM) and sufficient enough to produce a 60–150% increased invasion of Escherichia coli across brain microvascular endothelial cells (Chen et al., 2002). Whole animal studies also
n2:mentions: n3:21889975

Subject Item: _:vb16821795
rdf:type: n2:Context
rdf:value: This decrease in resistance is dose-dependent (0.1–100 μM) and sufficient enough to produce a 60–150% increased invasion of Escherichia coli across brain microvascular endothelial cells (Chen et al., >>2002<<). Whole animal studies also revealed nicotine-induced BBB dysfunction leading to increased transport from blood to brain of xenobiotics like squanivir, a protease inhibitor included in anti-retroviral therapy for HIV infection (Manda et
n2:mentions: n3:12174085

Subject Item: _:vb16821796
rdf:type: n2:Context
rdf:value: animal studies also revealed nicotine-induced BBB dysfunction leading to increased transport from blood to brain of xenobiotics like squanivir, a protease inhibitor included in anti-retroviral therapy for HIV infection (Manda et al., 2010a). These studies offer added insight into the consequences of nicotine use relating to uptake of therapeutics into the CNS.
n2:mentions: n3:20950334

Subject Item: _:vb16821797
rdf:type: n2:Context
rdf:value: Finally, both in vitro and in vivo studies report significant loss, or alterations in, tight junction proteins including ZO-1, claudin-3, JAMs, and occludin (Abbruscato et al., >>2002<<; Hawkins et al., 2004; Hutamekalin et al., 2008; Manda et al., 2010b).
n2:mentions: n3:12434396

Subject Item: _:vb16821798
rdf:type: n2:Context
rdf:value: Finally, both in vitro and in vivo studies report significant loss, or alterations in, tight junction proteins including ZO-1, claudin-3, JAMs, and occludin (Abbruscato et al., 2002; Hawkins et al., >>2004<<; Hutamekalin et al., 2008; Manda et al., 2010b).
n2:mentions: n3:15494156

Subject Item: _:vb16821799
rdf:type: n2:Context
rdf:value: Finally, both in vitro and in vivo studies report significant loss, or alterations in, tight junction proteins including ZO-1, claudin-3, JAMs, and occludin (Abbruscato et al., 2002; Hawkins et al., 2004; Hutamekalin et al., >>2008<<; Manda et al., 2010b).
n2:mentions: n3:17920942

Subject Item: _:vb16821800
rdf:type: n2:Context
rdf:value: in vitro and in vivo studies report significant loss, or alterations in, tight junction proteins including ZO-1, claudin-3, JAMs, and occludin (Abbruscato et al., 2002; Hawkins et al., 2004; Hutamekalin et al., 2008; Manda et al., 2010b).
n2:mentions: n3:20722969

Subject Item: _:vb16821801
rdf:type: n2:Context
rdf:value: Nicotine increases the activity of monocarboxylase and organic cation transporters while decreasing the functional activity of ion transporters like Na+, K+, 2Cl− co- transporter, and Na+, K+-ATPase on BECs (Wang et al., >>1994<<; Abbruscato et al., 2004; Lockman et al., 2005; Paulson et al., 2006; Liou et al., 2007).
n2:mentions: n3:8147886

Subject Item: _:vb16821802
rdf:type: n2:Context
rdf:value: the activity of monocarboxylase and organic cation transporters while decreasing the functional activity of ion transporters like Na+, K+, 2Cl− co- transporter, and Na+, K+-ATPase on BECs (Wang et al., 1994; Abbruscato et al., >>2004<<; Lockman et al., 2005; Paulson et al., 2006; Liou et al., 2007). Nicotine treatment produced a 22 and 17% decrease in Na+ and K+-ATPase activity in the microvasculature and brain, respectively (Wang et al., 1994).
n2:mentions: n3:15051802

Subject Item: _:vb16821803
rdf:type: n2:Context
rdf:value: monocarboxylase and organic cation transporters while decreasing the functional activity of ion transporters like Na+, K+, 2Cl− co- transporter, and Na+, K+-ATPase on BECs (Wang et al., 1994; Abbruscato et al., 2004; Lockman et al., >>2005<<; Paulson et al., 2006; Liou et al., 2007). Nicotine treatment produced a 22 and 17% decrease in Na+ and K+-ATPase activity in the microvasculature and brain, respectively (Wang et al., 1994).
n2:mentions: n3:15953347

Subject Item: _:vb16821804
rdf:type: n2:Context
rdf:value: organic cation transporters while decreasing the functional activity of ion transporters like Na+, K+, 2Cl− co- transporter, and Na+, K+-ATPase on BECs (Wang et al., 1994; Abbruscato et al., 2004; Lockman et al., 2005; Paulson et al., >>2006<<; Liou et al., 2007). Nicotine treatment produced a 22 and 17% decrease in Na+ and K+-ATPase activity in the microvasculature and brain, respectively (Wang et al., 1994).
n2:mentions: n3:16174793

Subject Item: _:vb16821805
rdf:type: n2:Context
rdf:value: while decreasing the functional activity of ion transporters like Na+, K+, 2Cl− co- transporter, and Na+, K+-ATPase on BECs (Wang et al., 1994; Abbruscato et al., 2004; Lockman et al., 2005; Paulson et al., 2006; Liou et al., >>2007<<). Nicotine treatment produced a 22 and 17% decrease in Na+ and K+-ATPase activity in the microvasculature and brain, respectively (Wang et al., 1994).
n2:mentions: n3:17689566

Subject Item: _:vb16821806
rdf:type: n2:Context
rdf:value: Nicotine treatment produced a 22 and 17% decrease in Na+ and K+-ATPase activity in the microvasculature and brain, respectively (Wang et al., >>1994<<). Nicotine also inhibited the activity of P-glycoprotein, an important efflux transporter responsible for impeding the entry of a range of compounds into the CNS (Manda et al., 2010a). Changes in transport mechanisms across the BBB can
n2:mentions: n3:8147886

Subject Item: _:vb16821807
rdf:type: n2:Context
rdf:value: Nicotine also inhibited the activity of P-glycoprotein, an important efflux transporter responsible for impeding the entry of a range of compounds into the CNS (Manda et al., 2010a). Changes in transport mechanisms across the BBB can produce detrimental alterations in ion gradients and in the nutrients available to the brain (Paulson et al., 2006; Yang et al., 2006). Nicotine-induced alterations in ion transport are
n2:mentions: n3:20950334

Subject Item: _:vb16821808
rdf:type: n2:Context
rdf:value: Changes in transport mechanisms across the BBB can produce detrimental alterations in ion gradients and in the nutrients available to the brain (Paulson et al., >>2006<<; Yang et al., 2006).
n2:mentions: n3:16174793

Subject Item: _:vb16821809
rdf:type: n2:Context
rdf:value: Changes in transport mechanisms across the BBB can produce detrimental alterations in ion gradients and in the nutrients available to the brain (Paulson et al., 2006; Yang et al., >>2006<<). Nicotine-induced alterations in ion transport are especially injurious as changes in ion gradients lead to brain edema lasting for up to 3 weeks after nicotine exposure as well as increased cerebral ischemic injury (Wang et al., 1997;
n2:mentions: n3:16450214

Subject Item: _:vb16821810
rdf:type: n2:Context
rdf:value: Nicotine-induced alterations in ion transport are especially injurious as changes in ion gradients lead to brain edema lasting for up to 3 weeks after nicotine exposure as well as increased cerebral ischemic injury (Wang et al., >>1997<<; Paulson et al., 2010). nAChRs on cells within the BBB are also affected by nicotine.
n2:mentions: n3:9040492

Subject Item: _:vb16821811
rdf:type: n2:Context
rdf:value: alterations in ion transport are especially injurious as changes in ion gradients lead to brain edema lasting for up to 3 weeks after nicotine exposure as well as increased cerebral ischemic injury (Wang et al., 1997; Paulson et al., >>2010<<). nAChRs on cells within the BBB are also affected by nicotine. Chronic nicotine decreases nAChR surface expression as well as expression of certain nAChR subunits, particularly the α2 isoform, on BECs (Wang et al., 1994; Abbruscato et al.
n2:mentions: n3:19889792

Subject Item: _:vb16821812
rdf:type: n2:Context
rdf:value: Chronic nicotine decreases nAChR surface expression as well as expression of certain nAChR subunits, particularly the α2 isoform, on BECs (Wang et al., >>1994<<; Abbruscato et al., 2004; Lockman et al., 2005).
n2:mentions: n3:8147886

Subject Item: _:vb16821813
rdf:type: n2:Context
rdf:value: Chronic nicotine decreases nAChR surface expression as well as expression of certain nAChR subunits, particularly the α2 isoform, on BECs (Wang et al., 1994; Abbruscato et al., >>2004<<; Lockman et al., 2005).
n2:mentions: n3:15051802

Subject Item: _:vb16821814
rdf:type: n2:Context
rdf:value: Chronic nicotine decreases nAChR surface expression as well as expression of certain nAChR subunits, particularly the α2 isoform, on BECs (Wang et al., 1994; Abbruscato et al., 2004; Lockman et al., >>2005<<). While nicotine activity at nAChRs on BECs alters the BBB, treatment with nAChRs antagonists (e.g., mecamylamine, α-bungarotoxin, and hexamethonium) decreases nicotine-induced BBB dysfunction. This decrease in BBB disruption was
n2:mentions: n3:15953347

Subject Item: _:vb16821815
rdf:type: n2:Context
rdf:value: This decrease in BBB disruption was identified by attenuation of [14C]sucrose leakage into the brain parenchyma, reversal of ZO-1 loss, and decreased Escherichia coli invasion in an in vitro BBB model (Abbruscato et al., >>2002<<; Chen et al., 2002; Conklin et al., 2002; Hawkins et al., 2005; see Table 4 for a summary of the effects of nicotine on BBB function).
n2:mentions: n3:12434396

Subject Item: _:vb16821816
rdf:type: n2:Context
rdf:value: decrease in BBB disruption was identified by attenuation of [14C]sucrose leakage into the brain parenchyma, reversal of ZO-1 loss, and decreased Escherichia coli invasion in an in vitro BBB model (Abbruscato et al., 2002; Chen et al., >>2002<<; Conklin et al., 2002; Hawkins et al., 2005; see Table 4 for a summary of the effects of nicotine on BBB function).
n2:mentions: n3:12174085

Subject Item: _:vb16821817
rdf:type: n2:Context
rdf:value: was identified by attenuation of [14C]sucrose leakage into the brain parenchyma, reversal of ZO-1 loss, and decreased Escherichia coli invasion in an in vitro BBB model (Abbruscato et al., 2002; Chen et al., 2002; Conklin et al., >>2002<<; Hawkins et al., 2005; see Table 4 for a summary of the effects of nicotine on BBB function).
n2:mentions: n3:11839560

Subject Item: _:vb16821818
rdf:type: n2:Context
rdf:value: attenuation of [14C]sucrose leakage into the brain parenchyma, reversal of ZO-1 loss, and decreased Escherichia coli invasion in an in vitro BBB model (Abbruscato et al., 2002; Chen et al., 2002; Conklin et al., 2002; Hawkins et al., >>2005<<; see Table 4 for a summary of the effects of nicotine on BBB function).
n2:mentions: n3:15708958

Subject Item: _:vb16821819
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (>>2011<<); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al.
n2:mentions: n3:21889975

Subject Item: _:vb16821820
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (>>2008<<); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al.
n2:mentions: n3:17920942

Subject Item: _:vb16821821
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (>>1992<<); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al.
n2:mentions: n3:1521035

Subject Item: _:vb16821822
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (>>2002<<); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999);
n2:mentions: n3:12434396

Subject Item: _:vb16821823
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (>>2002<<); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992);
n2:mentions: n3:12174085

Subject Item: _:vb16821824
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (>>2004<<); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997);
n2:mentions: n3:15354631

Subject Item: _:vb16821825
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (>>2002<<); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010);
n2:mentions: n3:11904622

Subject Item: _:vb16821826
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al.
n2:mentions: n3:20950334

Subject Item: _:vb16821827
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011);
n2:mentions: n3:20722969

Subject Item: _:vb16821828
rdf:type: n2:Context
rdf:value: 1Rodriguez-Gaztelumendi et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (>>2007<<); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al.
n2:mentions: n3:17689566

Subject Item: _:vb16821829
rdf:type: n2:Context
rdf:value: et al. (2011); 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (>>2006<<); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al.
n2:mentions: n3:16450214

Subject Item: _:vb16821830
rdf:type: n2:Context
rdf:value: 2Hutamekalin et al. (2008); 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (>>2006<<); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al.
n2:mentions: n3:16174793

Subject Item: _:vb16821831
rdf:type: n2:Context
rdf:value: 3Schilling et al. (1992); 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (>>2004<<); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al.
n2:mentions: n3:15051802

Subject Item: _:vb16821832
rdf:type: n2:Context
rdf:value: 4Abbruscato et al. (2002); 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (>>2005<<); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:15708958

Subject Item: _:vb16821833
rdf:type: n2:Context
rdf:value: 5Chen et al. (2002); 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (>>1999<<); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:10479471

Subject Item: _:vb16821834
rdf:type: n2:Context
rdf:value: 6Albaugh et al. (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (>>1992<<); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:1420090

Subject Item: _:vb16821835
rdf:type: n2:Context
rdf:value: (2004); 7Speer et al. (2002); 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (>>1997<<); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:9040492

Subject Item: _:vb16821836
rdf:type: n2:Context
rdf:value: 8Manda et al. (2010a,b); 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (>>2010<<); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:19889792

Subject Item: _:vb16821837
rdf:type: n2:Context
rdf:value: 9Liou et al. (2007); 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (>>2011<<); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:21239632

Subject Item: _:vb16821838
rdf:type: n2:Context
rdf:value: 10Yang et al. (2006); 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (>>2009<<); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:19433117

Subject Item: _:vb16821839
rdf:type: n2:Context
rdf:value: 11Paulson et al. (2006); 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (>>2005<<); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:15953347

Subject Item: _:vb16821840
rdf:type: n2:Context
rdf:value: 12Abbruscato et al. (2004); 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (>>1994<<); 22Gerzanich et al. (2003); 23Yong et al. (1997).
n2:mentions: n3:8147886

Subject Item: _:vb16821841
rdf:type: n2:Context
rdf:value: 13Hawkins et al. (2005); 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (>>2003<<); 23Yong et al. (1997).
n2:mentions: n3:14724353

Subject Item: _:vb16821842
rdf:type: n2:Context
rdf:value: 14Uzum et al. (1999); 15Lin et al. (1992); 16Wang et al. (1997); 17Paulson et al. (2010); 18Bradford et al. (2011); 19Canis et al. (2009); 20Lockman et al. (2005); 21Wang et al. (1994); 22Gerzanich et al. (2003); 23Yong et al. (>>1997<<).
n2:mentions: n3:9413272

Subject Item: _:vb16821843
rdf:type: n2:Context
rdf:value: Nicotine enhances peripheral blood mononuclear cell migration across cerebral vessels through a cascade promoting increased expression of adhesion molecules and inflammatory cytokines (Yong et al., >>1997<<; Albaugh et al., 2004; Bradford et al., 2011).
n2:mentions: n3:9413272

Subject Item: _:vb16821844
rdf:type: n2:Context
rdf:value: Nicotine enhances peripheral blood mononuclear cell migration across cerebral vessels through a cascade promoting increased expression of adhesion molecules and inflammatory cytokines (Yong et al., 1997; Albaugh et al., >>2004<<; Bradford et al., 2011).
n2:mentions: n3:15354631

Subject Item: _:vb16821845
rdf:type: n2:Context
rdf:value: enhances peripheral blood mononuclear cell migration across cerebral vessels through a cascade promoting increased expression of adhesion molecules and inflammatory cytokines (Yong et al., 1997; Albaugh et al., 2004; Bradford et al., >>2011<<). The expression of ICAM-1, VCAM-1, and P-selectin is increased with chronic nicotine treatment (Yong et al., 1997; Albaugh et al., 2004).
n2:mentions: n3:21239632

Subject Item: _:vb16821846
rdf:type: n2:Context
rdf:value: The expression of ICAM-1, VCAM-1, and P-selectin is increased with chronic nicotine treatment (Yong et al., >>1997<<; Albaugh et al., 2004).
n2:mentions: n3:9413272

Subject Item: _:vb16821847
rdf:type: n2:Context
rdf:value: The expression of ICAM-1, VCAM-1, and P-selectin is increased with chronic nicotine treatment (Yong et al., 1997; Albaugh et al., >>2004<<). Furthermore, nicotine increases gene expression of TNFα, IL-18, IL-1β, and chemokines including CCL2, CCL8, and CXC3CL1 (Bradford et al., 2011). Nicotine also decreases gene expression of anti-inflammatory factors (e.g., Bcl6, IL-10,
n2:mentions: n3:15354631

Subject Item: _:vb16821848
rdf:type: n2:Context
rdf:value: Furthermore, nicotine increases gene expression of TNFα, IL-18, IL-1β, and chemokines including CCL2, CCL8, and CXC3CL1 (Bradford et al., >>2011<<). Nicotine also decreases gene expression of anti-inflammatory factors (e.g., Bcl6, IL-10, and CCL25; Bradford et al., 2011). These studies indicate that nicotine increases the expression of inflammatory cytokines and endothelial adhesion
n2:mentions: n3:21239632

Subject Item: _:vb16821849
rdf:type: n2:Context
rdf:value: Nicotine also decreases gene expression of anti-inflammatory factors (e.g., Bcl6, IL-10, and CCL25; Bradford et al., >>2011<<). These studies indicate that nicotine increases the expression of inflammatory cytokines and endothelial adhesion molecules and can enhance leukocyte migration across the BBB, particularly during neuroinflammation.
n2:mentions: n3:21239632

Subject Item: _:vb16821850
rdf:type: n5:Section
dc:title: stimulant co-morbidity with hiv infection
n5:contains: _:vb16821900 _:vb16821901 _:vb16821902 _:vb16821903 _:vb16821896 _:vb16821897 _:vb16821898 _:vb16821899 _:vb16821892 _:vb16821893 _:vb16821894 _:vb16821895 _:vb16821888 _:vb16821889 _:vb16821890 _:vb16821891 _:vb16821852 _:vb16821853 _:vb16821854 _:vb16821855 _:vb16821851 _:vb16821868 _:vb16821869 _:vb16821870 _:vb16821871 _:vb16821864 _:vb16821865 _:vb16821866 _:vb16821867 _:vb16821860 _:vb16821861 _:vb16821862 _:vb16821863 _:vb16821856 _:vb16821857 _:vb16821858 _:vb16821859 _:vb16821884 _:vb16821885 _:vb16821886 _:vb16821887 _:vb16821880 _:vb16821881 _:vb16821882 _:vb16821883 _:vb16821876 _:vb16821877 _:vb16821878 _:vb16821879 _:vb16821872 _:vb16821873 _:vb16821874 _:vb16821875

Subject Item: _:vb16821851
rdf:type: n2:Context
rdf:value: Studies report that meth abuse is linked with enhanced frequency of unprotected sex and increased HIV transmission (Semple et al., >>2004<<; Buchacz et al., 2005).
n2:mentions: n3:15135564

Subject Item: _:vb16821852
rdf:type: n2:Context
rdf:value: Studies report that meth abuse is linked with enhanced frequency of unprotected sex and increased HIV transmission (Semple et al., 2004; Buchacz et al., >>2005<<). Moreover, the morbidity and mortality of meth-abusing HIV-positive individuals far exceeds that seen with either pathology alone.
n2:mentions: n3:16103774

Subject Item: _:vb16821853
rdf:type: n2:Context
rdf:value: HIV infects peripheral leukocytes which migrate across the BBB, thus allowing the virus access to the CNS (An et al., >>1999<<). This migration occurs early in HIV infection (Risdahl et al., 1998; Romanelli et al., 2006) though HIV-induced toxicity of BECs occurs throughout infection and parallels HIV toxicity of neurons (Price et al., 2005).
n2:mentions: n3:10560658

Subject Item: _:vb16821854
rdf:type: n2:Context
rdf:value: This migration occurs early in HIV infection (Risdahl et al., >>1998<<; Romanelli et al., 2006) though HIV-induced toxicity of BECs occurs throughout infection and parallels HIV toxicity of neurons (Price et al., 2005).
n2:mentions: n3:9610668

Subject Item: _:vb16821855
rdf:type: n2:Context
rdf:value: This migration occurs early in HIV infection (Risdahl et al., 1998; Romanelli et al., >>2006<<) though HIV-induced toxicity of BECs occurs throughout infection and parallels HIV toxicity of neurons (Price et al., 2005).
n2:mentions: n3:16881008

Subject Item: _:vb16821856
rdf:type: n2:Context
rdf:value: This migration occurs early in HIV infection (Risdahl et al., 1998; Romanelli et al., 2006) though HIV-induced toxicity of BECs occurs throughout infection and parallels HIV toxicity of neurons (Price et al., >>2005<<). Once HIV-infected cells enter the brain, HIV-produced proteins trigger neuroinflammation which can exacerbate the neuroinflammatory effects of stimulant drugs. As overviewed above, stimulant drug abuse compromises BBB integrity through
n2:mentions: n3:15910762

Subject Item: _:vb16821857
rdf:type: n2:Context
rdf:value: Meth increases the expression of HIV co-receptors, CXCR4 and CCR5 (Nair et al., >>2009<<), and can significantly increase HIV replication in astrocytes (Gavrilin et al., 2002).
n2:mentions: n3:18958626

Subject Item: _:vb16821858
rdf:type: n2:Context
rdf:value: Meth increases the expression of HIV co-receptors, CXCR4 and CCR5 (Nair et al., 2009), and can significantly increase HIV replication in astrocytes (Gavrilin et al., >>2002<<). In HIV-positive meth abusers, meth-induced BBB dysfunction facilitates increased transport of HIV-infected leukocytes into the brain (Liang et al., 2008).
n2:mentions: n3:12053278

Subject Item: _:vb16821859
rdf:type: n2:Context
rdf:value: In HIV-positive meth abusers, meth-induced BBB dysfunction facilitates increased transport of HIV-infected leukocytes into the brain (Liang et al., >>2008<<). Moreover, HIV-induced BBB damage might increase the concentration of meth within the CNS contributing to further meth-neurotoxicity. Co-treatment of meth and HIV protein gp120 decreases transendothelial electrical resistance across BECs
n2:mentions: n3:18458095

Subject Item: _:vb16821860
rdf:type: n2:Context
rdf:value: Co-treatment of meth and HIV protein gp120 decreases transendothelial electrical resistance across BECs more than treatment with meth or gp120 alone (Mahajan et al., >>2008<<). Administration of meth and gp120 or the HIV protein Tat in combination, further decreased the expression of ZO-1, claudin-3, claudin-5, and JAM-2 than either treatment alone (Mahajan et al., 2008; Banerjee et al., 2010). In addition to
n2:mentions: n3:18329007

Subject Item: _:vb16821861
rdf:type: n2:Context
rdf:value: Administration of meth and gp120 or the HIV protein Tat in combination, further decreased the expression of ZO-1, claudin-3, claudin-5, and JAM-2 than either treatment alone (Mahajan et al., >>2008<<; Banerjee et al., 2010).
n2:mentions: n3:18329007

Subject Item: _:vb16821862
rdf:type: n2:Context
rdf:value: Administration of meth and gp120 or the HIV protein Tat in combination, further decreased the expression of ZO-1, claudin-3, claudin-5, and JAM-2 than either treatment alone (Mahajan et al., 2008; Banerjee et al., >>2010<<). In addition to the effects of meth and HIV on tight junction proteins, increased levels of MMP-2 and MMP-9 were reported with meth and Tat treatment in an in vitro BBB model (Conant et al., 2004) and in the cerebrospinal fluid of
n2:mentions: n3:20188164

Subject Item: _:vb16821863
rdf:type: n2:Context
rdf:value: In addition to the effects of meth and HIV on tight junction proteins, increased levels of MMP-2 and MMP-9 were reported with meth and Tat treatment in an in vitro BBB model (Conant et al., >>2004<<) and in the cerebrospinal fluid of HIV-positive individuals (Conant et al., 1999; Liuzzi et al., 2004).
n2:mentions: n3:14982725

Subject Item: _:vb16821864
rdf:type: n2:Context
rdf:value: HIV on tight junction proteins, increased levels of MMP-2 and MMP-9 were reported with meth and Tat treatment in an in vitro BBB model (Conant et al., 2004) and in the cerebrospinal fluid of HIV-positive individuals (Conant et al., >>1999<<; Liuzzi et al., 2004). These peptidases can produce persistent BBB damage, leaving the brain open to prolonged infiltration of HIV and other peripheral toxins.
n2:mentions: n3:10482270

Subject Item: _:vb16821865
rdf:type: n2:Context
rdf:value: proteins, increased levels of MMP-2 and MMP-9 were reported with meth and Tat treatment in an in vitro BBB model (Conant et al., 2004) and in the cerebrospinal fluid of HIV-positive individuals (Conant et al., 1999; Liuzzi et al., >>2004<<). These peptidases can produce persistent BBB damage, leaving the brain open to prolonged infiltration of HIV and other peripheral toxins.
n2:mentions: n3:14662518

Subject Item: _:vb16821866
rdf:type: n2:Context
rdf:value: Chang et al. (>>2005<<) found increased neuronal loss in frontal gray matter (−5.7%), frontal white matter (−6.1%), and basal ganglia (−6%) when compared with HIV-positive meth-naïve individuals and HIV-negative meth abusers.
n2:mentions: n3:15677602

Subject Item: _:vb16821867
rdf:type: n2:Context
rdf:value: These studies also reported increased glial activation and changes in cellular metabolism in frontal white matter and basal ganglia in HIV-positive meth abusers (Chang et al., >>2005<<). Meth-induced glial activation may lead to increased progression of neuroAIDS in HIV-positive meth abusers (Garden, 2002). DA neurotoxicity is associated with both meth abuse, and HIV infection appears worsened by the combination (Czub
n2:mentions: n3:15677602

Subject Item: _:vb16821868
rdf:type: n2:Context
rdf:value: Meth-induced glial activation may lead to increased progression of neuroAIDS in HIV-positive meth abusers (Garden, >>2002<<). DA neurotoxicity is associated with both meth abuse, and HIV infection appears worsened by the combination (Czub et al., 2001; Maragos et al., 2002; Theodore et al., 2006). Increased DA neurotoxicity with meth abuse and HIV/AIDS
n2:mentions: n3:12379911

Subject Item: _:vb16821869
rdf:type: n2:Context
rdf:value: DA neurotoxicity is associated with both meth abuse, and HIV infection appears worsened by the combination (Czub et al., >>2001<<; Maragos et al., 2002; Theodore et al., 2006).
n2:mentions: n3:11271377

Subject Item: _:vb16821870
rdf:type: n2:Context
rdf:value: DA neurotoxicity is associated with both meth abuse, and HIV infection appears worsened by the combination (Czub et al., 2001; Maragos et al., >>2002<<; Theodore et al., 2006).
n2:mentions: n3:12421368

Subject Item: _:vb16821871
rdf:type: n2:Context
rdf:value: DA neurotoxicity is associated with both meth abuse, and HIV infection appears worsened by the combination (Czub et al., 2001; Maragos et al., 2002; Theodore et al., >>2006<<). Increased DA neurotoxicity with meth abuse and HIV/AIDS co-morbidity may increase the risk of DA-associated disorders like PD. In fact, meth abusers have a twofold increase in developing PD compared with healthy controls or cocaine
n2:mentions: n3:16338084

Subject Item: _:vb16821872
rdf:type: n2:Context
rdf:value: In fact, meth abusers have a twofold increase in developing PD compared with healthy controls or cocaine abusers (Callaghan et al., >>2012<<) and as many as 10% of patients with HAND also display Parkinsonian features (Berger and Nath, 1997).
n2:mentions: n3:21794992

Subject Item: _:vb16821873
rdf:type: n2:Context
rdf:value: In fact, meth abusers have a twofold increase in developing PD compared with healthy controls or cocaine abusers (Callaghan et al., 2012) and as many as 10% of patients with HAND also display Parkinsonian features (Berger and Nath, >>1997<<). In summary, the neuropathological features associated with both meth abuse and HIV/AIDS may be exacerbated through meth-induced BBB dysfunction resulting in, or worsened by, neuroinflammation.
n2:mentions: n3:9450229

Subject Item: _:vb16821874
rdf:type: n2:Context
rdf:value: Similar to meth abuse, individuals abusing MDMA are more likely to engage in risky sexual behaviors and injection drug use (Dunn et al., >>2010<<). Indeed, 77% of participants in a clinical investigation reported not using condoms when under the influence of MDMA, and of this group, 54% reported having two or more sexual partners during this time (Dunn et al., 2010).
n2:mentions: n3:19781861

Subject Item: _:vb16821875
rdf:type: n2:Context
rdf:value: Indeed, 77% of participants in a clinical investigation reported not using condoms when under the influence of MDMA, and of this group, 54% reported having two or more sexual partners during this time (Dunn et al., >>2010<<). In a similar clinical study, 9.3% of MDMA users surveyed reported having unprotected sex with partners who were either HIV-positive or of unknown HIV status (Klitzman et al., 2002). These behaviors likely increase HIV transmission
n2:mentions: n3:19781861

Subject Item: _:vb16821876
rdf:type: n2:Context
rdf:value: In a similar clinical study, 9.3% of MDMA users surveyed reported having unprotected sex with partners who were either HIV-positive or of unknown HIV status (Klitzman et al., >>2002<<). These behaviors likely increase HIV transmission within this population (Mitcheson et al., 2008). Little is currently known about the neurotoxic implications of MDMA and HIV co-morbidity. As MDMA produces BBB dysfunction as well as
n2:mentions: n3:11906799

Subject Item: _:vb16821877
rdf:type: n2:Context
rdf:value: These behaviors likely increase HIV transmission within this population (Mitcheson et al., >>2008<<). Little is currently known about the neurotoxic implications of MDMA and HIV co-morbidity. As MDMA produces BBB dysfunction as well as neuroinflammation and oxidative stress, which both perpetuate BBB damage, MDMA-induced BBB dysfunction
n2:mentions: n3:18638703

Subject Item: _:vb16821878
rdf:type: n2:Context
rdf:value: Early investigations reported cocaine abuse as a risk factor for increased HIV transmission and a more rapid progression to AIDS (Fiala et al., >>1998<<; Webber et al., 1999). Cocaine increases HIV infiltration into the CNS through increased HIV-infected leukocyte adhesion and transmigration across the BBB endothelium.
n2:mentions: n3:9666272

Subject Item: _:vb16821879
rdf:type: n2:Context
rdf:value: Early investigations reported cocaine abuse as a risk factor for increased HIV transmission and a more rapid progression to AIDS (Fiala et al., 1998; Webber et al., >>1999<<). Cocaine increases HIV infiltration into the CNS through increased HIV-infected leukocyte adhesion and transmigration across the BBB endothelium.
n2:mentions: n3:10202832

Subject Item: _:vb16821880
rdf:type: n2:Context
rdf:value: Cocaine also increases HIV replication in monocytes, macrophages, and astrocytes (Peterson et al., >>1991<<; Roth et al., 2002; Reynolds et al., 2006).
n2:mentions: n3:1984454

Subject Item: _:vb16821881
rdf:type: n2:Context
rdf:value: Cocaine also increases HIV replication in monocytes, macrophages, and astrocytes (Peterson et al., 1991; Roth et al., >>2002<<; Reynolds et al., 2006).
n2:mentions: n3:11865430

Subject Item: _:vb16821882
rdf:type: n2:Context
rdf:value: Cocaine also increases HIV replication in monocytes, macrophages, and astrocytes (Peterson et al., 1991; Roth et al., 2002; Reynolds et al., >>2006<<). This is especially important as astrocytes may act as a reservoir for HIV within the brain (Nath, 2010). Preclinical studies revealed that cocaine enhances oxidative stress, neuronal dysfunction, and apoptosis in gp120 and Tat-treated
n2:mentions: n3:17034766

Subject Item: _:vb16821883
rdf:type: n2:Context
rdf:value: This is especially important as astrocytes may act as a reservoir for HIV within the brain (Nath, >>2010<<). Preclinical studies revealed that cocaine enhances oxidative stress, neuronal dysfunction, and apoptosis in gp120 and Tat-treated cells in vitro and in rodents (Koutsilieri et al., 1997; Nath et al., 2000; Bagetta et al., 2004). Recent
n2:mentions: n3:20201849

Subject Item: _:vb16821884
rdf:type: n2:Context
rdf:value: Preclinical studies revealed that cocaine enhances oxidative stress, neuronal dysfunction, and apoptosis in gp120 and Tat-treated cells in vitro and in rodents (Koutsilieri et al., >>1997<<; Nath et al., 2000; Bagetta et al., 2004).
n2:mentions: n3:9372455

Subject Item: _:vb16821885
rdf:type: n2:Context
rdf:value: Preclinical studies revealed that cocaine enhances oxidative stress, neuronal dysfunction, and apoptosis in gp120 and Tat-treated cells in vitro and in rodents (Koutsilieri et al., 1997; Nath et al., >>2000<<; Bagetta et al., 2004).
n2:mentions: n3:10665489

Subject Item: _:vb16821886
rdf:type: n2:Context
rdf:value: Preclinical studies revealed that cocaine enhances oxidative stress, neuronal dysfunction, and apoptosis in gp120 and Tat-treated cells in vitro and in rodents (Koutsilieri et al., 1997; Nath et al., 2000; Bagetta et al., >>2004<<). Recent findings from Napier et al. (2010) revealed that cocaine and Tat synergize to over activate cortical neurons. Like cocaine, Tat can inhibit DAT which may contribute to HIV-induced DA neurotoxicity (Aksenov et al., 2008). When
n2:mentions: n3:15036625

Subject Item: _:vb16821887
rdf:type: n2:Context
rdf:value: Like cocaine, Tat can inhibit DAT which may contribute to HIV-induced DA neurotoxicity (Aksenov et al., >>2008<<). When combined, cocaine plus Tat may result in DA neurotoxicities which exacerbate HIV neuropathology. Cocaine-induced BBB dysfunction leading to increased HIV transmission into the CNS is apt to contribute to the resulting
n2:mentions: n3:18606182

Subject Item: _:vb16821888
rdf:type: n2:Context
rdf:value: Cocaine abuse accelerates HIV disease progression by decreasing CD4+ T-cell counts and increasing HIV viral load, independent of anti-retroviral therapies (Baum et al., >>2009<<). Chaisson et al. (1989) found that daily cocaine use increased the risk of HIV infection up to sixfold in African American and Hispanic populations. Persistent cocaine abusers are also three times more likely to die from AIDS-related
n2:mentions: n3:19295339

Subject Item: _:vb16821889
rdf:type: n2:Context
rdf:value: Chaisson et al. (>>1989<<) found that daily cocaine use increased the risk of HIV infection up to sixfold in African American and Hispanic populations.
n2:mentions: n3:2909798

Subject Item: _:vb16821890
rdf:type: n2:Context
rdf:value: Persistent cocaine abusers are also three times more likely to die from AIDS-related complications than cocaine-naïve individuals (Cook et al., >>2008<<). This suggests a synergistic interaction between cocaine and HIV which exacerbates HIV disease progression. Interactions between cocaine and HIV within the brain parenchyma may be enhanced through cocaine-induced increases in
n2:mentions: n3:18580615

Subject Item: _:vb16821891
rdf:type: n2:Context
rdf:value: Studies report a 51% or higher cigarette smoking rate among nationally surveyed HIV-positive individuals (Collins et al., >>2001<<; Gritz et al., 2004; Burkhalter et al., 2005).
n2:mentions: n3:11570649

Subject Item: _:vb16821892
rdf:type: n2:Context
rdf:value: Studies report a 51% or higher cigarette smoking rate among nationally surveyed HIV-positive individuals (Collins et al., 2001; Gritz et al., >>2004<<; Burkhalter et al., 2005).
n2:mentions: n3:14982690

Subject Item: _:vb16821893
rdf:type: n2:Context
rdf:value: Studies report a 51% or higher cigarette smoking rate among nationally surveyed HIV-positive individuals (Collins et al., 2001; Gritz et al., 2004; Burkhalter et al., >>2005<<). Though little is known about the effects of nicotine on HIV disease progression, smoking increases the likelihood of HIV-related complications (e.g., bacterial pneumonia and HIV-associated dementia) and increases the mortality rate of
n2:mentions: n3:16085522

Subject Item: _:vb16821894
rdf:type: n2:Context
rdf:value: on HIV disease progression, smoking increases the likelihood of HIV-related complications (e.g., bacterial pneumonia and HIV-associated dementia) and increases the mortality rate of HIV-positive individuals (Hirschtick et al., >>1995<<; Conley et al., 1996; Feldman et al., 2006). Furthermore, nicotine can act as a major immunosuppressive agent by attenuating the immune and virological response to anti-retroviral therapies by up to 40% (Humfleet et al., 2009).
n2:mentions: n3:7651475

Subject Item: _:vb16821895
rdf:type: n2:Context
rdf:value: progression, smoking increases the likelihood of HIV-related complications (e.g., bacterial pneumonia and HIV-associated dementia) and increases the mortality rate of HIV-positive individuals (Hirschtick et al., 1995; Conley et al., >>1996<<; Feldman et al., 2006). Furthermore, nicotine can act as a major immunosuppressive agent by attenuating the immune and virological response to anti-retroviral therapies by up to 40% (Humfleet et al., 2009).
n2:mentions: n3:8874629

Subject Item: _:vb16821896
rdf:type: n2:Context
rdf:value: increases the likelihood of HIV-related complications (e.g., bacterial pneumonia and HIV-associated dementia) and increases the mortality rate of HIV-positive individuals (Hirschtick et al., 1995; Conley et al., 1996; Feldman et al., >>2006<<). Furthermore, nicotine can act as a major immunosuppressive agent by attenuating the immune and virological response to anti-retroviral therapies by up to 40% (Humfleet et al., 2009).
n2:mentions: n3:16670229

Subject Item: _:vb16821897
rdf:type: n2:Context
rdf:value: Furthermore, nicotine can act as a major immunosuppressive agent by attenuating the immune and virological response to anti-retroviral therapies by up to 40% (Humfleet et al., >>2009<<). Nicotine has both pro- and anti-inflammatory properties. The immunosuppressive effects of nicotine include increasing T-cell unresponsiveness, increasing IL-4 production, and inhibiting the production of certain pro-inflammatory
n2:mentions: n3:19537954

Subject Item: _:vb16821898
rdf:type: n2:Context
rdf:value: The immunosuppressive effects of nicotine include increasing T-cell unresponsiveness, increasing IL-4 production, and inhibiting the production of certain pro-inflammatory cytokines (Sopori and Kozak, >>1998<<). Immunosuppressive functions can add to the already detrimental immune suppression produced by HIV infection leading to an accelerated progression of HIV-associated complications. The pro-inflammatory effects of nicotine within the CNS
n2:mentions: n3:9610683

Subject Item: _:vb16821899
rdf:type: n2:Context
rdf:value: Nicotine enhances the production of HIV in macrophages (Abbud et al., >>1995<<) and in activated microglia (Rock et al., 2008).
n2:mentions: n3:7658083

Subject Item: _:vb16821900
rdf:type: n2:Context
rdf:value: Nicotine enhances the production of HIV in macrophages (Abbud et al., 1995) and in activated microglia (Rock et al., >>2008<<). Similar increases in HIV replication are also seen with opiate and cocaine abuse which are reported to promote HIV neuropathology (Nath et al., 2002; Roth et al., 2005). The scope of what is currently known about the effects of nicotine
n2:mentions: n3:18060582

Subject Item: _:vb16821901
rdf:type: n2:Context
rdf:value: Similar increases in HIV replication are also seen with opiate and cocaine abuse which are reported to promote HIV neuropathology (Nath et al., >>2002<<; Roth et al., 2005).
n2:mentions: n3:12394784

Subject Item: _:vb16821902
rdf:type: n2:Context
rdf:value: Similar increases in HIV replication are also seen with opiate and cocaine abuse which are reported to promote HIV neuropathology (Nath et al., 2002; Roth et al., >>2005<<). The scope of what is currently known about the effects of nicotine on HIV disease progression is limited, though HIV-positive individuals who smoke cigarettes show a decreased immune response, poorer responses to anti-retroviral
n2:mentions: n3:16204638

Subject Item: _:vb16821903
rdf:type: n2:Context
rdf:value: HIV-positive individuals who smoke cigarettes show a decreased immune response, poorer responses to anti-retroviral therapies, greater risk of viral rebound, and an increased probability for HIV-related complications (Feldman et al., >>2006<<). Nicotine may increase HIV infiltration into the CNS through nicotine-induced BBB dysfunction and increase HIV replication within microglia in the brain to accelerate progression to neuroAIDS.
n2:mentions: n3:16670229

Subject Item: _:vb497081526
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 5
n2:hasRelevantPaperId: n3:19897082

Subject Item: _:vb497081527
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 4
n2:hasRelevantPaperId: n3:21148086

Subject Item: _:vb497081528
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 4
n2:hasRelevantPaperId: n3:11519485

Subject Item: _:vb497081529
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:22551810

Subject Item: _:vb497081530
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:22714667

Subject Item: _:vb497081531
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:17105918

Subject Item: _:vb497081532
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:25209871

Subject Item: _:vb497081533
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:19506719

Subject Item: _:vb497081534
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:16036808

Subject Item: _:vb497081535
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:25644383

Subject Item: _:vb497081536
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:18430470

Subject Item: _:vb497081537
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:18046654

Subject Item: _:vb497081538
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:18509037

Subject Item: _:vb497081539
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:21738771

Subject Item: _:vb497081540
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:23251514

Subject Item: _:vb497081541
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:15914466

Subject Item: _:vb497081542
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:22048062

Subject Item: _:vb497081543
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:19897075

Subject Item: _:vb497081544
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:9666272

Subject Item: _:vb497081545
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:19319745

Subject Item: _:vb497081546
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:19233481

Subject Item: _:vb497081547
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:1746528

Subject Item: _:vb497081548
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:20976166

Subject Item: _:vb497081549
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:19654589

Subject Item: _:vb497081550
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:25999807

Subject Item: _:vb497081551
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:22316499

Subject Item: _:vb497081552
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:23456305

Subject Item: _:vb497081553
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11724929

Subject Item: _:vb497081554
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19738171

Subject Item: _:vb497081555
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23079813

Subject Item: _:vb497081556
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25873042

Subject Item: _:vb497081557
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:8258759

Subject Item: _:vb497081558
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24486327

Subject Item: _:vb497081559
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25788874

Subject Item: _:vb497081560
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15036625

Subject Item: _:vb497081561
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24892744

Subject Item: _:vb497081562
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:1685745

Subject Item: _:vb497081563
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:17976544

Subject Item: _:vb497081564
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18215617

Subject Item: _:vb497081565
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21426580

Subject Item: _:vb497081566
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21595923

Subject Item: _:vb497081567
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21786077

Subject Item: _:vb497081568
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23084084

Subject Item: _:vb497081569
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:9278385

Subject Item: _:vb497081570
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11865430

Subject Item: _:vb497081571
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21040844

Subject Item: _:vb497081572
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21303698

Subject Item: _:vb497081573
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25268786

Subject Item: _:vb497081574
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:27402494

Subject Item: _:vb497081575
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:2909798

Subject Item: _:vb497081576
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:17914061

Subject Item: _:vb497081577
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18097880

Subject Item: _:vb497081578
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24894206

Subject Item: _:vb497081579
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25691383

Subject Item: _:vb497081580
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:26539167

Subject Item: _:vb497081581
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:56036

Subject Item: _:vb497081582
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10602399

Subject Item: _:vb497081583
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:12684743

Subject Item: _:vb497081584
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25945248

Subject Item: _:vb497081585
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:1574543

Subject Item: _:vb497081586
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15808355

Subject Item: _:vb497081587
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15962513

Subject Item: _:vb497081588
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16685256

Subject Item: _:vb497081589
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25529562

Subject Item: _:vb497081590
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11106749

Subject Item: _:vb497081591
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11729018

Subject Item: _:vb497081592
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19743454

Subject Item: _:vb497081593
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20953917

Subject Item: _:vb497081594
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21792905

Subject Item: _:vb497081595
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16557263

Subject Item: _:vb497081596
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:17848967

Subject Item: _:vb497081597
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19462243

Subject Item: _:vb497081598
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21399909

Subject Item: _:vb497081599
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23039106

Subject Item: _:vb497081600
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24391808

Subject Item: _:vb497081601
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:8728048

Subject Item: _:vb497081602
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10618285

Subject Item: _:vb497081603
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18240064

Subject Item: _:vb497081604
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23547924

Subject Item: _:vb497081605
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23721877

Subject Item: _:vb497081606
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19306229

Subject Item: _:vb497081607
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20492508

Subject Item: _:vb497081608
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:22817991

Subject Item: _:vb497081609
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:26661236

Subject Item: _:vb497081610
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15976090

Subject Item: _:vb497081611
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10864098

Subject Item: _:vb497081612
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16251831

Subject Item: _:vb497081613
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:22934772

Subject Item: _:vb497081614
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:8809853

Subject Item: _:vb497081615
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10454636

Subject Item: _:vb497081616
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16153175

Subject Item: _:vb497081617
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18305237

Subject Item: _:vb497081618
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18991854

Subject Item: _:vb497081619
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19630745

Subject Item: _:vb497081620
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20624003

Subject Item: _:vb497081621
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:22820108

Subject Item: _:vb497081622
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11309629

Subject Item: _:vb497081623
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15977641

Subject Item: _:vb497081624
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25175865

Subject Item: _:vb497081625
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:26283916

Subject Item: _:vb497081626
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:28344073

Subject Item: _:vb497081627
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21900636

Subject Item: _:vb497081628
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25613133

Subject Item: _:vb497081629
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:28441414

Subject Item: _:vb497081630
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:28851615

Subject Item: _:vb497081631
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:2820058

Subject Item: _:vb497081632
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:14982725

Subject Item: _:vb497081633
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16386305

Subject Item: _:vb497081634
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24359561

Subject Item: _:vb497081635
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24867611

Subject Item: _:vb497081636
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25973614

Subject Item: _:vb497081637
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:1604712

Subject Item: _:vb497081638
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:8011238

Subject Item: _:vb497081639
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:9498303

Subject Item: _:vb497081640
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10550317

Subject Item: _:vb497081641
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19025481

Subject Item: _:vb497081642
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20396973

Subject Item: _:vb497081643
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11754990

Subject Item: _:vb497081644
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19287189

Subject Item: _:vb497081645
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:22591363

Subject Item: _:vb497081646
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:22947176

Subject Item: _:vb497081647
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:12438433

Subject Item: _:vb497081648
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10822328

Subject Item: _:vb497081649
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25175867

Subject Item: _:vb497081650
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25377444

Subject Item: _:vb497081651
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:14713949

Subject Item: _:vb497081652
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16790532

Subject Item: _:vb497081653
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18265929

Subject Item: _:vb497081654
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18941231

Subject Item: _:vb497081655
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20201848

Subject Item: _:vb497081656
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:12707054

Subject Item: _:vb497081657
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16644490

Subject Item: _:vb497081658
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18709468

Subject Item: _:vb497081659
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18991959

Subject Item: _:vb497081660
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20517932

Subject Item: _:vb497081661
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21508219

Subject Item: _:vb497081662
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:12551932

Subject Item: _:vb497081663
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20668216

Subject Item: _:vb497081664
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21219914

Subject Item: _:vb497081665
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24267647

Subject Item: _:vb497081666
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24424383

Subject Item: _:vb497081667
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25862193

Subject Item: _:vb497081668
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19606280

Subject Item: _:vb497081669
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21810934

Subject Item: _:vb497081670
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24625401

Subject Item: _:vb497081671
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15519244

Subject Item: _:vb497081672
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19364908

Subject Item: _:vb497081673
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19543960

Subject Item: _:vb497081674
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10358063

Subject Item: _:vb497081675
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16086684

Subject Item: _:vb497081676
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16796601

Subject Item: _:vb497081677
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15207256

Subject Item: _:vb497081678
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21174240