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Find video protocols related to scientific articles indexed in Pubmed.
Overexpression of membrane-bound fas ligand (CD95L) exacerbates autoimmune disease and renal pathology in pristane-induced lupus.
J. Immunol.
PUBLISHED: 08-05-2013
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Loss-of-function mutations in the Fas death receptor or its ligand result in a lymphoproliferative syndrome and exacerbate clinical disease in most lupus-prone strains of mice. One exception is mice injected with 2,6,10,14-tetramethylpentadecane (TMPD), a hydrocarbon oil commonly known as pristane, which induces systemic lupus erythematosus-like disease. Although Fas/Fas ligand (FasL) interactions have been strongly implicated in the activation-induced cell death of both lymphocytes and other APCs, FasL can also trigger the production of proinflammatory cytokines. FasL is a transmembrane protein with a matrix metalloproteinase cleavage site in the ectodomain. Matrix metalloproteinase cleavage inactivates membrane-bound FasL and releases a soluble form reported to have both antagonist and agonist activity. To better understand the impact of FasL cleavage on both the proapoptotic and proinflammatory activity of FasL, its cleavage site was deleted through targeted mutation to produce the deleted cleavage site (?CS) mouse line. ?CS mice express higher levels of membrane-bound FasL than do wild-type mice and fail to release soluble FasL. To determine to what extent FasL promotes inflammation in lupus mice, TMPD-injected FasL-deficient and ?CS BALB/c mice were compared with control TMPD-injected BALB/c mice. We found that FasL deficiency significantly reduced the early inflammatory exudate induced by TMPD injection. In contrast, ?CS mice developed a markedly exacerbated disease profile associated with a higher frequency of splenic neutrophils and macrophages, a profound change in anti-nuclear Ab specificity, and markedly increased proteinuria and kidney pathology compared with controls. These results demonstrate that FasL promotes inflammation in TMPD-induced autoimmunity, and its cleavage limits FasL proinflammatory activity.
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The genome of Anopheles darlingi, the main neotropical malaria vector.
Osvaldo Marinotti, Gustavo C Cerqueira, Luiz Gonzaga Paula de Almeida, Maria Inês Tiraboschi Ferro, Élgion Lúcio da Silva Loreto, Arnaldo Zaha, Santuza M R Teixeira, Adam R Wespiser, Alexandre Almeida E Silva, Aline Daiane Schlindwein, Ana Carolina Landim Pacheco, Artur Luiz da Costa da Silva, Brenton R Graveley, Brian P Walenz, Bruna de Araujo Lima, Carlos Alexandre Gomes Ribeiro, Carlos Gustavo Nunes-Silva, Carlos Roberto de Carvalho, Célia Maria de Almeida Soares, Claudia Beatriz Afonso de Menezes, Cleverson Matiolli, Daniel Caffrey, Demetrius Antonio M Araújo, Diana Magalhaes de Oliveira, Douglas Golenbock, Edmundo Carlos Grisard, Fabiana Fantinatti-Garboggini, Fabíola Marques de Carvalho, Fernando Gomes Barcellos, Francisco Prosdocimi, Gemma May, Gilson Martins de Azevedo Junior, Giselle Moura Guimarães, Gustavo Henrique Goldman, Itácio Q M Padilha, Jacqueline da Silva Batista, Jesus Aparecido Ferro, José M C Ribeiro, Juliana Lopes Rangel Fietto, Karina Maia Dabbas, Louise Cerdeira, Lucymara Fassarella Agnez-Lima, Marcelo Brocchi, Marcos Oliveira de Carvalho, Marcus de Melo Teixeira, Maria de Mascena Diniz Maia, Maria Helena S Goldman, Maria Paula Cruz Schneider, Maria Sueli Soares Felipe, Mariangela Hungria, Marisa Fabiana Nicolás, Maristela Pereira, Martín Alejandro Montes, Mauricio E Cantão, Michel Vincentz, Míriam Silva Rafael, Neal Silverman, Patrícia Hermes Stoco, Rangel Celso Souza, Renato Vicentini, Ricardo Tostes Gazzinelli, Rogério de Oliveira Neves, Rosane Silva, Spartaco Astolfi-Filho, Talles Eduardo Ferreira Maciel, Turán P Urményi, Wanderli Pedro Tadei, Erney Plessmann Camargo, Ana Tereza Ribeiro de Vasconcelos.
Nucleic Acids Res.
PUBLISHED: 06-12-2013
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Anopheles darlingi is the principal neotropical malaria vector, responsible for more than a million cases of malaria per year on the American continent. Anopheles darlingi diverged from the African and Asian malaria vectors ?100 million years ago (mya) and successfully adapted to the New World environment. Here we present an annotated reference A. darlingi genome, sequenced from a wild population of males and females collected in the Brazilian Amazon. A total of 10 481 predicted protein-coding genes were annotated, 72% of which have their closest counterpart in Anopheles gambiae and 21% have highest similarity with other mosquito species. In spite of a long period of divergent evolution, conserved gene synteny was observed between A. darlingi and A. gambiae. More than 10 million single nucleotide polymorphisms and short indels with potential use as genetic markers were identified. Transposable elements correspond to 2.3% of the A. darlingi genome. Genes associated with hematophagy, immunity and insecticide resistance, directly involved in vector-human and vector-parasite interactions, were identified and discussed. This study represents the first effort to sequence the genome of a neotropical malaria vector, and opens a new window through which we can contemplate the evolutionary history of anopheline mosquitoes. It also provides valuable information that may lead to novel strategies to reduce malaria transmission on the South American continent. The A. darlingi genome is accessible at www.labinfo.lncc.br/index.php/anopheles-darlingi.
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RNA helicase signaling is critical for type i interferon production and protection against Rift Valley fever virus during mucosal challenge.
J. Virol.
PUBLISHED: 02-13-2013
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Rift Valley fever virus (RVFV) is an emerging RNA virus with devastating economic and social consequences. Clinically, RVFV induces a gamut of symptoms ranging from febrile illness to retinitis, hepatic necrosis, hemorrhagic fever, and death. It is known that type I interferon (IFN) responses can be protective against severe pathology; however, it is unknown which innate immune receptor pathways are crucial for mounting this response. Using both in vitro assays and in vivo mucosal mouse challenge, we demonstrate here that RNA helicases are critical for IFN production by immune cells and that signaling through the helicase adaptor molecule MAVS (mitochondrial antiviral signaling) is protective against mortality and more subtle pathology during RVFV infection. In addition, we demonstrate that Toll-like-receptor-mediated signaling is not involved in IFN production, further emphasizing the importance of the RNA cellular helicases in type I IFN responses to RVFV.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.