<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>29(2)</volume><submitter>Gupta RK</submitter><pubmed_abstract>&lt;h4>Background and purpose&lt;/h4>Neuroinflammatory molecules, including tumor necrosis factor-alpha, interleukin1-beta, lymphocyte function associated molecule-1, and intercellular cell adhesion molecule-1 contribute to the development of brain abscess. We hypothesized that the high fractional anisotropy (FA) in the brain abscess cavity reflects the upregulation of these neuroinflammatory molecules.&lt;h4>Materials and methods&lt;/h4>Diffusion tensor imaging (DTI) was performed in 24 patients with brain abscess and Staphylococcus aureus-treated as well as nontreated Jurket cell lines (at 4 time points: 1, 24, 48, and 72 hours). Neuroinflammatory molecules were quantified from the brain abscess cavity aspirate of the patients as well as from the heat-killed S aureus-treated and nontreated cell line</pubmed_abstract><journal>AJNR. American journal of neuroradiology</journal><pagination>326-32</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8118972</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>In vivo demonstration of neuroinflammatory molecule expression in brain abscess with diffusion tensor imaging.</pubmed_title><pmcid>PMC8118972</pmcid><pubmed_authors>Gupta RK</pubmed_authors><pubmed_authors>Srivastava C</pubmed_authors><pubmed_authors>Khetan P</pubmed_authors><pubmed_authors>Trivedi R</pubmed_authors><pubmed_authors>Prasad A</pubmed_authors><pubmed_authors>Narayana PA</pubmed_authors><pubmed_authors>Nath K</pubmed_authors><pubmed_authors>Rathore RK</pubmed_authors><pubmed_authors>Prasad KN</pubmed_authors><pubmed_authors>Husain N</pubmed_authors><pubmed_authors>Husain M</pubmed_authors></additional><is_claimable>false</is_claimable><name>In vivo demonstration of neuroinflammatory molecule expression in brain abscess with diffusion tensor imaging.</name><description>&lt;h4>Background and purpose&lt;/h4>Neuroinflammatory molecules, including tumor necrosis factor-alpha, interleukin1-beta, lymphocyte function associated molecule-1, and intercellular cell adhesion molecule-1 contribute to the development of brain abscess. We hypothesized that the high fractional anisotropy (FA) in the brain abscess cavity reflects the upregulation of these neuroinflammatory molecules.&lt;h4>Materials and methods&lt;/h4>Diffusion tensor imaging (DTI) was performed in 24 patients with brain abscess and Staphylococcus aureus-treated as well as nontreated Jurket cell lines (at 4 time points: 1, 24, 48, and 72 hours). Neuroinflammatory molecules were quantified from the brain abscess cavity aspirate of the patients as well as from the heat-killed S aureus-treated and nontreated cell line</description><dates><release>2008-01-01T00:00:00Z</release><publication>2008 Feb</publication><modification>2025-04-26T07:21:58.302Z</modification><creation>2022-02-10T10:01:50.403Z</creation></dates><accession>S-EPMC8118972</accession><cross_references><pubmed>17989372</pubmed><doi>10.3174/ajnr.A0826</doi><doi>10.3174/ajnr.a0826</doi></cross_references></HashMap>