Base de dados : MEDLINE
Pesquisa : A10.802 [Categoria DeCS]
Referências encontradas : 8173 [refinar]
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  1 / 8173 MEDLINE  
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[PMID]:28453760
[Au] Autor:Hibiya S; Tsuchiya K; Hayashi R; Fukushima K; Horita N; Watanabe S; Shirasaki T; Nishimura R; Kimura N; Nishimura T; Gotoh N; Oshima S; Okamoto R; Nakamura T; Watanabe M
[Ad] Endereço:Department of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
[Ti] Título:Long-term Inflammation Transforms Intestinal Epithelial Cells of Colonic Organoids.
[So] Source:J Crohns Colitis;11(5):621-630, 2017 May 01.
[Is] ISSN:1876-4479
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background and Aims: Patients with ulcerative colitis [UC] are at an increased risk of developing colitis-associated cancer [CAC], suggesting that continuous inflammation in the colon promotes the transformation of colonic epithelial cells. However, the mechanisms underlying cell transformation in UC remain unknown. We therefore aimed to investigate the effect of long-term inflammation on intestinal epithelial cells [IECs] using organoid culture. Methods: IECs were isolated from mouse colon, and were cultured according to a method for a three-dimensional [3D] organoid culture. To mimic chronic inflammation, a mixture of cytokines and bacterial components were added to the medium for over a year. Cell signal intensity was assessed by 3D immunofluorescence. Cell transformation was assessed by microarray with gene set enrichment analysis. Results: Stimulation with cytokines resulted in a significant induction of target genes for the nuclear factor [NF]-κB pathway in colonic organoids. Following 60 weeks of continuous stimulation, cell differentiation was suppressed. Continuous stimulation also resulted in significant amplification of NF-κB signalling. Amplified NF-κB signalling by long-term stimulation remained in colonic organoids even 11 weeks after the removal of all cytokines. Some genes were specifically upregulated only in colonic organoids after the removal all cytokines following long-term stimulation. Conclusions: Colonic organoids stimulated with cytokines for a prolonged period were established as in vitro model to assess long-term epithelial responses to inflammatory cytokines. Chronic inflammation led to sustained NF-κB signalling activation in colonic organoids, resulting in cell transformation that might be related to the carcinogenesis of CAC in UC.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/patologia
Colite/patologia
Mucosa Intestinal/citologia
Organoides/patologia
[Mh] Termos MeSH secundário: Animais
Colo/citologia
Colo/patologia
Citocinas/metabolismo
Feminino
Mucosa Intestinal/patologia
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (NF-kappa B)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/ecco-jcc/jjw186


  2 / 8173 MEDLINE  
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[PMID]:28468837
[Au] Autor:Lu W; Rettenmeier E; Paszek M; Yueh MF; Tukey RH; Trottier J; Barbier O; Chen S
[Ad] Endereço:Laboratory of Environmental Toxicology, Department of Pharmacology, University of California, San Diego, La Jolla, California (W.L., E.R., M.P., M-F.Y., R.H.T., S.C.); and Laboratory of Molecular Pharmacology, CHU de Quebec Research Centre and Faculty of Pharmacy, Laval University, Québec (Québec),
[Ti] Título:Crypt Organoid Culture as an in Vitro Model in Drug Metabolism and Cytotoxicity Studies.
[So] Source:Drug Metab Dispos;45(7):748-754, 2017 Jul.
[Is] ISSN:1521-009X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The gastrointestinal tract is enriched with xenobiotic processing proteins that play important roles in xenobiotic bioactivation, metabolism, and detoxification. The application of genetically modified mouse models has been instrumental in characterizing the function of xenobiotic processing genes (XPG) and their proteins in drug metabolism. Here, we report the utilization of three-dimensional crypt organoid cultures from these animal models to study intestinal drug metabolism and toxicity. With the successful culturing of crypt organoids, we profiled the abundance of Phase I and Phase II XPG expression, drug transporter gene expression, and xenobiotic nuclear receptor (XNR) gene expression. Functions of XNRs were examined by treating crypt cells with XNR prototypical agonists. Real-time quantitative polymerase chain reaction demonstrated that the representative downstream target genes were induced. These findings were validated from cultures developed from XNR-null mice. In crypt cultures isolated from mice, pregnenolone 16 -carbonitrile failed to induce gene expression; similarly, WY14643 failed to induce in the crypts. Crypt cultures from control ( ) and intestinal epithelial cell (IEC) specific null mice ( ) were treated with camptothecin-11, an anticancer prodrug with severe intestinal toxicity that originates from insufficient UGT1A1-dependent glucuronidation of its active metabolite SN-38. In the absence of gene expression, crypt cultures exhibit very limited production of SN-38 glucuronide, concordant with increased apoptosis in comparison with crypt cultures. This study suggests crypt organoid cultures as an effective in vitro model for studying intestinal drug metabolism and toxicity.
[Mh] Termos MeSH primário: Camptotecina/análogos & derivados
Inativação Metabólica/fisiologia
Organoides/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Camptotecina/metabolismo
Técnicas de Cultura de Células/métodos
Citocromo P-450 CYP3A/metabolismo
Expressão Gênica/fisiologia
Intestinos/metabolismo
Taxa de Depuração Metabólica/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Xenobióticos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Xenobiotics); 7673326042 (irinotecan); EC 1.14.14.1 (Cytochrome P-450 CYP3A); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1124/dmd.117.075945


  3 / 8173 MEDLINE  
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[PMID]:28467818
[Au] Autor:Janda CY; Dang LT; You C; Chang J; de Lau W; Zhong ZA; Yan KS; Marecic O; Siepe D; Li X; Moody JD; Williams BO; Clevers H; Piehler J; Baker D; Kuo CJ; Garcia KC
[Ad] Endereço:Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, and Department of Structural Biology, Stanford University School of Medicine, Stanford, California 94305, USA.
[Ti] Título:Surrogate Wnt agonists that phenocopy canonical Wnt and ß-catenin signalling.
[So] Source:Nature;545(7653):234-237, 2017 05 11.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Wnt proteins modulate cell proliferation and differentiation and the self-renewal of stem cells by inducing ß-catenin-dependent signalling through the Wnt receptor frizzled (FZD) and the co-receptors LRP5 and LRP6 to regulate cell fate decisions and the growth and repair of several tissues. The 19 mammalian Wnt proteins are cross-reactive with the 10 FZD receptors, and this has complicated the attribution of distinct biological functions to specific FZD and Wnt subtype interactions. Furthermore, Wnt proteins are modified post-translationally by palmitoylation, which is essential for their secretion, function and interaction with FZD receptors. As a result of their acylation, Wnt proteins are very hydrophobic and require detergents for purification, which presents major obstacles to the preparation and application of recombinant Wnt proteins. This hydrophobicity has hindered the determination of the molecular mechanisms of Wnt signalling activation and the functional importance of FZD subtypes, and the use of Wnt proteins as therapeutic agents. Here we develop surrogate Wnt agonists, water-soluble FZD-LRP5/LRP6 heterodimerizers, with FZD5/FZD8-specific and broadly FZD-reactive binding domains. Similar to WNT3A, these Wnt agonists elicit a characteristic ß-catenin signalling response in a FZD-selective fashion, enhance the osteogenic lineage commitment of primary mouse and human mesenchymal stem cells, and support the growth of a broad range of primary human organoid cultures. In addition, the surrogates can be systemically expressed and exhibit Wnt activity in vivo in the mouse liver, regulating metabolic liver zonation and promoting hepatocyte proliferation, resulting in hepatomegaly. These surrogates demonstrate that canonical Wnt signalling can be activated by bi-specific ligands that induce receptor heterodimerization. Furthermore, these easily produced, non-lipidated Wnt surrogate agonists facilitate functional studies of Wnt signalling and the exploration of Wnt agonists for translational applications in regenerative medicine.
[Mh] Termos MeSH primário: Transdução de Sinais
Proteínas Wnt/agonistas
Proteínas Wnt/metabolismo
Via de Sinalização Wnt
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Linhagem da Célula
Proliferação Celular
Receptores Frizzled/metabolismo
Células HEK293
Hepatócitos/citologia
Hepatomegalia/metabolismo
Hepatomegalia/patologia
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Intestinos/citologia
Ligantes
Fígado/metabolismo
Fígado/patologia
Proteína-5 Relacionada a Receptor de Lipoproteína de Baixa Densidade/metabolismo
Proteína-6 Relacionada a Receptor de Lipoproteína de Baixa Densidade/metabolismo
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Camundongos
Modelos Moleculares
Organoides/citologia
Organoides/metabolismo
Multimerização Proteica
Solubilidade
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Frizzled Receptors); 0 (Ligands); 0 (Low Density Lipoprotein Receptor-Related Protein-5); 0 (Low Density Lipoprotein Receptor-Related Protein-6); 0 (Wnt Proteins); 0 (beta Catenin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180217
[Lr] Data última revisão:
180217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/nature22306


  4 / 8173 MEDLINE  
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[PMID]:28455349
[Au] Autor:Chen KY; Srinivasan T; Tung KL; Belmonte JM; Wang L; Murthy PKL; Choi J; Rakhilin N; King S; Varanko AK; Witherspoon M; Nishimura N; Glazier JA; Lipkin SM; Bu P; Shen X
[Ad] Endereço:School of Electrical and Computer Engineering, Cornell University, Ithaca, NY, USA.
[Ti] Título:A Notch positive feedback in the intestinal stem cell niche is essential for stem cell self-renewal.
[So] Source:Mol Syst Biol;13(4):927, 2017 Apr 28.
[Is] ISSN:1744-4292
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The intestinal epithelium is the fastest regenerative tissue in the body, fueled by fast-cycling stem cells. The number and identity of these dividing and migrating stem cells are maintained by a mosaic pattern at the base of the crypt. How the underlying regulatory scheme manages this dynamic stem cell niche is not entirely clear. We stimulated intestinal organoids with Notch ligands and inhibitors and discovered that intestinal stem cells employ a positive feedback mechanism via direct Notch binding to the second intron of the Notch1 gene. Inactivation of the positive feedback by CRISPR/Cas9 mutation of the binding sequence alters the mosaic stem cell niche pattern and hinders regeneration in organoids. Dynamical system analysis and agent-based multiscale stochastic modeling suggest that the positive feedback enhances the robustness of Notch-mediated niche patterning. This study highlights the importance of feedback mechanisms in spatiotemporal control of the stem cell niche.
[Mh] Termos MeSH primário: Retroalimentação Fisiológica
Intestinos/citologia
Receptor Notch1/genética
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Autorrenovação Celular
Seres Humanos
Intestinos/metabolismo
Camundongos
Mutação
Organoides/metabolismo
Receptor Notch1/química
Transdução de Sinais
Nicho de Células-Tronco
Processos Estocásticos
Biologia de Sistemas/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LGR5 protein, human); 0 (NOTCH1 protein, human); 0 (Receptor, Notch1); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.15252/msb.20167324


  5 / 8173 MEDLINE  
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[PMID]:28467820
[Au] Autor:Yan KS; Janda CY; Chang J; Zheng GXY; Larkin KA; Luca VC; Chia LA; Mah AT; Han A; Terry JM; Ootani A; Roelf K; Lee M; Yuan J; Li X; Bolen CR; Wilhelmy J; Davies PS; Ueno H; von Furstenberg RJ; Belgrader P; Ziraldo SB; Ordonez H; Henning SJ; Wong MH; Snyder MP; Weissman IL; Hsueh AJ; Mikkelsen TS; Garcia KC; Kuo CJ
[Ad] Endereço:Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.
[Ti] Título:Non-equivalence of Wnt and R-spondin ligands during Lgr5 intestinal stem-cell self-renewal.
[So] Source:Nature;545(7653):238-242, 2017 05 11.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The canonical Wnt/ß-catenin signalling pathway governs diverse developmental, homeostatic and pathological processes. Palmitoylated Wnt ligands engage cell-surface frizzled (FZD) receptors and LRP5 and LRP6 co-receptors, enabling ß-catenin nuclear translocation and TCF/LEF-dependent gene transactivation. Mutations in Wnt downstream signalling components have revealed diverse functions thought to be carried out by Wnt ligands themselves. However, redundancy between the 19 mammalian Wnt proteins and 10 FZD receptors and Wnt hydrophobicity have made it difficult to attribute these functions directly to Wnt ligands. For example, individual mutations in Wnt ligands have not revealed homeostatic phenotypes in the intestinal epithelium-an archetypal canonical, Wnt pathway-dependent, rapidly self-renewing tissue, the regeneration of which is fueled by proliferative crypt Lgr5 intestinal stem cells (ISCs). R-spondin ligands (RSPO1-RSPO4) engage distinct LGR4-LGR6, RNF43 and ZNRF3 receptor classes, markedly potentiate canonical Wnt/ß-catenin signalling, and induce intestinal organoid growth in vitro and Lgr5 ISCs in vivo. However, the interchangeability, functional cooperation and relative contributions of Wnt versus RSPO ligands to in vivo canonical Wnt signalling and ISC biology remain unknown. Here we identify the functional roles of Wnt and RSPO ligands in the intestinal crypt stem-cell niche. We show that the default fate of Lgr5 ISCs is to differentiate, unless both RSPO and Wnt ligands are present. However, gain-of-function studies using RSPO ligands and a new non-lipidated Wnt analogue reveal that these ligands have qualitatively distinct, non-interchangeable roles in ISCs. Wnt proteins are unable to induce Lgr5 ISC self-renewal, but instead confer a basal competency by maintaining RSPO receptor expression that enables RSPO ligands to actively drive and specify the extent of stem-cell expansion. This functionally non-equivalent yet cooperative interaction between Wnt and RSPO ligands establishes a molecular precedent for regulation of mammalian stem cells by distinct priming and self-renewal factors, with broad implications for precise control of tissue regeneration.
[Mh] Termos MeSH primário: Autorrenovação Celular
Intestinos/citologia
Receptores Acoplados a Proteínas-G/metabolismo
Células-Tronco/citologia
Células-Tronco/metabolismo
Trombospondinas/metabolismo
Proteínas Wnt/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Proliferação Celular
Feminino
Seres Humanos
Ligantes
Masculino
Camundongos
Organoides/citologia
Organoides/crescimento & desenvolvimento
Análise de Célula Única
Nicho de Células-Tronco
Transcriptoma
Ubiquitina-Proteína Ligases/metabolismo
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (LGR5 protein, human); 0 (Ligands); 0 (Receptors, G-Protein-Coupled); 0 (Thrombospondins); 0 (Wnt Proteins); 0 (beta Catenin); EC 2.3.2.27 (RNF43 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.3.2.27 (Znrf3 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/nature22313


  6 / 8173 MEDLINE  
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[PMID]:28745625
[Au] Autor:Merenda A; Andersson-Rolf A; Mustata RC; Li T; Kim H; Koo BK
[Ad] Endereço:Wellcome Trust - Medical Research Council Stem Cell Institute, University of Cambridge; Department of Genetics, University of Cambridge.
[Ti] Título:A Protocol for Multiple Gene Knockout in Mouse Small Intestinal Organoids Using a CRISPR-concatemer.
[So] Source:J Vis Exp;(125), 2017 Jul 12.
[Is] ISSN:1940-087X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CRISPR/Cas9 technology has greatly improved the feasibility and speed of loss-of-function studies that are essential in understanding gene function. In higher eukaryotes, paralogous genes can mask a potential phenotype by compensating the loss of a gene, thus limiting the information that can be obtained from genetic studies relying on single gene knockouts. We have developed a novel, rapid cloning method for guide RNA (gRNA) concatemers in order to create multi-gene knockouts following a single round of transfection in mouse small intestinal organoids. Our strategy allows for the concatemerization of up to four individual gRNAs into a single vector by performing a single Golden Gate shuffling reaction with annealed gRNA oligos and a pre-designed retroviral vector. This allows either the simultaneous knockout of up to four different genes, or increased knockout efficiency following the targeting of one gene by multiple gRNAs. In this protocol, we show in detail how to efficiently clone multiple gRNAs into the retroviral CRISPR-concatemer vector and how to achieve highly efficient electroporation in intestinal organoids. As an example, we show that simultaneous knockout of two pairs of genes encoding negative regulators of the Wnt signaling pathway (Axin1/2 and Rnf43/Znrf3) renders intestinal organoids resistant to the withdrawal of key growth factors.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas/genética
Repetições Palindrômicas Curtas Agrupadas e Regularmente Espaçadas/genética
Técnicas de Inativação de Genes/métodos
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Knockout
Organoides
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.3791/55916


  7 / 8173 MEDLINE  
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[PMID]:28461408
[Au] Autor:Picco G; Garnett MJ
[Ad] Endereço:Wellcome Trust Sanger Institute, Cambridge, United Kingdom.
[Ti] Título:A Road Map for Precision Cancer Medicine Using Personalized Models.
[So] Source:Cancer Discov;7(5):456-458, 2017 05.
[Is] ISSN:2159-8290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo: A study by Pauli and colleagues in this issue of describes the creation of a precision cancer platform for patients with advanced disease, integrating DNA sequencing of patient tumors with the generation of patient-derived organoids and xenografts. They propose the use of this platform for drug testing to nominate therapeutic options for individual patients and for therapeutic biomarker discovery. .
[Mh] Termos MeSH primário: Neoplasias
Medicina de Precisão
[Mh] Termos MeSH secundário: Xenoenxertos
Seres Humanos
Organoides
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1158/2159-8290.CD-17-0268


  8 / 8173 MEDLINE  
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[PMID]:29215633
[Au] Autor:Jager M; Blokzijl F; Sasselli V; Boymans S; Janssen R; Besselink N; Clevers H; van Boxtel R; Cuppen E
[Ad] Endereço:Center for Molecular Medicine and Oncode Institute, University Medical Center Utrecht, Utrecht University, Utrecht, the Netherlands.
[Ti] Título:Measuring mutation accumulation in single human adult stem cells by whole-genome sequencing of organoid cultures.
[So] Source:Nat Protoc;13(1):59-78, 2018 Jan.
[Is] ISSN:1750-2799
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Characterization of mutational processes in adult stem cells (ASCs) will improve our understanding of aging-related diseases, such as cancer and organ failure, and may ultimately help prevent the development of these diseases. Here, we present a method for cataloging mutations in individual human ASCs without the necessity of using error-prone whole-genome amplification. Single ASCs are expanded in vitro into clonal organoid cultures to generate sufficient DNA for accurate whole-genome sequencing (WGS) analysis. We developed a data-analysis pipeline that identifies with high confidence somatic variants that accumulated in vivo in the original ASC. These genome-wide mutation catalogs are valuable resources for the characterization of the underlying mutational mechanisms. In addition, this protocol can be used to determine the effects of culture conditions or mutagen exposure on mutation accumulation in ASCs in vitro. Here, we describe a protocol for human liver ASCs that can be completed over a period of 3-4 months with hands-on time of ∼5 d.
[Mh] Termos MeSH primário: Células-Tronco Adultas/citologia
Acúmulo de Mutações
Mutação/genética
Organoides/citologia
Sequenciamento Completo do Genoma/métodos
[Mh] Termos MeSH secundário: Células Cultivadas
DNA/análise
DNA/genética
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Fígado/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9007-49-2 (DNA)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1038/nprot.2017.111


  9 / 8173 MEDLINE  
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[PMID]:29209702
[Au] Autor:Hampton T
[Ti] Título:Body-on-a-Chip Reveals Multitissue Interactions During Drug Exposure.
[So] Source:JAMA;318(21):2069-2070, 2017 Dec 05.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Modelos Biológicos
Organoides/efeitos dos fármacos
Farmacologia
Engenharia Tecidual/métodos
[Mh] Termos MeSH secundário: Seres Humanos
Miniaturização
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.17869


  10 / 8173 MEDLINE  
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[PMID]:28465333
[Au] Autor:Camp JG; Treutlein B
[Ad] Endereço:Evolutionary Genetics, Max Planck Institute for Evolutionary Anthropology, 04103 Leipzig, Germany.
[Ti] Título:Human organomics: a fresh approach to understanding human development using single-cell transcriptomics.
[So] Source:Development;144(9):1584-1587, 2017 05 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Innovative methods designed to recapitulate human organogenesis from pluripotent stem cells provide a means to explore human developmental biology. New technologies to sequence and analyze single-cell transcriptomes can deconstruct these 'organoids' into constituent parts, and reconstruct lineage trajectories during cell differentiation. In this Spotlight article we summarize the different approaches to performing single-cell transcriptomics on organoids, and discuss the opportunities and challenges of applying these techniques to generate organ-level, mechanistic models of human development and disease. Together, these technologies will move past characterization to the prediction of human developmental and disease-related phenomena.
[Mh] Termos MeSH primário: Perfilação da Expressão Gênica/métodos
Crescimento e Desenvolvimento
Organoides/metabolismo
Análise de Célula Única/métodos
[Mh] Termos MeSH secundário: Linhagem da Célula
Seres Humanos
Organoides/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1242/dev.150458



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde