Democracia como mestre de obras

3º congresso – As múltiplas Faces da Arquitetura Contemporânea de 2016 – As múltiplas Faces da Arquitetura Contemporânea – foram apresentados pelos/as estudantes da disciplina de Crítica e História da Arquitetura e da Cidade IV sob orientação da professora Andreia Moassab, do curso de Arquitetura e Urbanismo da Universidade Federal da Integração Latino-americana – UNILA. O congresso é parte da avaliação final da disciplina, no qual os/as estudantes apresentam a sua versão e dialogam com autores/as e textos de referência sobre a arquitetura nas últimas décadasConsiderando a questão de produção do espaço doméstico como uma forma de análise arquitetônica das décadas de 1960 e 1970, neste trabalho a autora trata este assunto mostrando as diversas formas de se pensar sobre os problemas existentes no mundo em relação a habitação, o uso cotidiano deste espaço por nós e como as considerações sobre isso mudaram bastante numa época marcada pelo inicio de uma revolução tecnológica apressadaUNIL

2021 Taxonomic update of phylum Negarnaviricota (Riboviria: Orthornavirae), including the large orders Bunyavirales and Mononegavirales.

Correction to: 2021 Taxonomic update of phylum Negarnaviricota (Riboviria: Orthornavirae), including the large orders Bunyavirales and Mononegavirales. Archives of Virology (2021) 166:3567–3579. https://doi.org/10.1007/s00705-021-05266-wIn March 2021, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote on newly proposed taxa, the phylum Negarnaviricota was amended and emended. The phylum was expanded by four families (Aliusviridae, Crepuscuviridae, Myriaviridae, and Natareviridae), three subfamilies (Alpharhabdovirinae, Betarhabdovirinae, and Gammarhabdovirinae), 42 genera, and 200 species. Thirty-nine species were renamed and/or moved and seven species were abolished. This article presents the updated taxonomy of Negarnaviricota as now accepted by the ICTV.This work was supported in part through Laulima Government Solutions, LLC prime contract with the US National Institute of Allergy and Infectious Diseases (NIAID) under Contract No. HHSN272201800013C. J.H.K. performed this work as an employee of Tunnell Government Services (TGS), a subcontractor of Laulima Government Solutions, LLC under Contract No. HHSN272201800013C. This work was also supported in part with federal funds from the National Cancer Institute (NCI), National Institutes of Health (NIH), under Contract No. 75N91019D00024, Task Order No. 75N91019F00130 to I.C., who was supported by the Clinical Monitoring Research Program Directorate, Frederick National Lab for Cancer Research. This work was also funded in part by Contract No. HSHQDC-15-C-00064 awarded by DHS S&T for the management and operation of The National Biodefense Analysis and Countermeasures Center, a federally funded research and development center operated by the Battelle National Biodefense Institute (V.W.); and NIH contract HHSN272201000040I/HHSN27200004/D04 and grant R24AI120942 (N.V., R.B.T.). S.S. acknowledges partial support from the Special Research Initiative of Mississippi Agricultural and Forestry Experiment Station (MAFES), Mississippi State University, and the National Institute of Food and Agriculture, US Department of Agriculture, Hatch Project 1021494. Part of this work was supported by the Francis Crick Institute which receives its core funding from Cancer Research UK (FC001030), the UK Medical Research Council (FC001030), and the Wellcome Trust (FC001030).S

Cross talk between Wnt/β-catenin and Irf8 in leukemia progression and drug resistance

Progression and disease relapse of chronic myeloid leukemia (CML) depends on leukemia-initiating cells (LIC) that resist treatment. Using mouse genetics and a BCR-ABL model of CML, we observed cross talk between Wnt/β-catenin signaling and the interferon-regulatory factor 8 (Irf8). In normal hematopoiesis, activation of β-catenin results in up-regulation of Irf8, which in turn limits oncogenic β-catenin functions. Self-renewal and myeloproliferation become dependent on β-catenin in Irf8-deficient animals that develop a CML-like disease. Combined Irf8 deletion and constitutive β-catenin activation result in progression of CML into fatal blast crisis, elevated leukemic potential of BCR-ABL–induced LICs, and Imatinib resistance. Interestingly, activated β-catenin enhances a preexisting Irf8-deficient gene signature, identifying β-catenin as an amplifier of progression-specific gene regulation in the shift of CML to blast crisis. Collectively, our data uncover Irf8 as a roadblock for β-catenin–driven leukemia and imply both factors as targets in combinatorial therapy

2021 Taxonomic update of phylum Negarnaviricota (Riboviria: Orthornavirae), including the large orders Bunyavirales and Mononegavirales.

In March 2021, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote on newly proposed taxa, the phylum Negarnaviricota was amended and emended. The phylum was expanded by four families (Aliusviridae, Crepuscuviridae, Myriaviridae, and Natareviridae), three subfamilies (Alpharhabdovirinae, Betarhabdovirinae, and Gammarhabdovirinae), 42 genera, and 200 species. Thirty-nine species were renamed and/or moved and seven species were abolished. This article presents the updated taxonomy of Negarnaviricota as now accepted by the ICTV

Annual (2023) taxonomic update of RNA-directed RNA polymerase-encoding negative-sense RNA viruses (realm Riboviria: kingdom Orthornavirae: phylum Negarnaviricota)

55 Pág.In April 2023, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote on newly proposed taxa, the phylum Negarnaviricota was amended and emended. The phylum was expanded by one new family, 14 new genera, and 140 new species. Two genera and 538 species were renamed. One species was moved, and four were abolished. This article presents the updated taxonomy of Negarnaviricota as now accepted by the ICTV.This work was supported in part through the Laulima Government Solutions, LLC, prime contract with the U.S. National Institute of Allergy and Infec tious Diseases (NIAID) under Contract No. HHSN272201800013C. J.H.K. performed this work as an employee of Tunnell Government Services (TGS), a subcontractor of Laulima Government Solutions, LLC, under Contract No. HHSN272201800013C. U.J.B. was supported by the Division of Intramural Resarch, NIAID. This work was also funded in part by Contract No. HSHQDC15-C-00064 awarded by DHS S and T for the management and operation of The National Biodefense Analysis and Countermeasures Centre, a federally funded research and development centre operated by the Battelle National Biodefense Institute (V.W.); and NIH contract HHSN272201000040I/HHSN27200004/D04 and grant R24AI120942 (N.V., R.B.T.). S.S. acknowl edges support from the Mississippi Agricultural and Forestry Experiment Station (MAFES), USDA-ARS project 58-6066-9-033 and the National Institute of Food and Agriculture, U.S. Department of Agriculture, Hatch Project, under Accession Number 1021494. The funders had no role in the design of the study; in the collection, analysis, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. The views and conclusions contained in this document are those of the authors and should not be interpreted as necessarily representing the official policies, either expressed or implied, of the U.S. Department of the Army, the U.S. Department of Defence, the U.S. Department of Health and Human Services, including the Centres for Disease Control and Prevention, the U.S. Department of Homeland Security (DHS) Science and Technology Directorate (S and T), or of the institutions and companies affiliated with the authors. In no event shall any of these entities have any responsibility or liability for any use, misuse, inability to use, or reliance upon the information contained herein. The U.S. departments do not endorse any products or commercial services mentioned in this publication. The U.S. Government retains and the publisher, by accepting the article for publication, acknowledges that the U.S.Government retains a non-exclusive, paid up, irrevocable, world-wide license to publish or reproduce the published form of this manuscript, or allow others to do so, for U.S. Government purposes.Peer reviewe

Using Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes as a Model to Study Trypanosoma cruzi Infection

Submitted by Nuzia Santos ([email protected]) on 2019-08-21T14:03:04Z No. of bitstreams: 1 Using Human Induced Pluripotent Stem .pdf: 1908077 bytes, checksum: 178f6efbded1fadb06946707daced99a (MD5)Approved for entry into archive by Nuzia Santos ([email protected]) on 2019-08-21T14:07:21Z (GMT) No. of bitstreams: 1 Using Human Induced Pluripotent Stem .pdf: 1908077 bytes, checksum: 178f6efbded1fadb06946707daced99a (MD5)Made available in DSpace on 2019-08-21T14:07:21Z (GMT). No. of bitstreams: 1 Using Human Induced Pluripotent Stem .pdf: 1908077 bytes, checksum: 178f6efbded1fadb06946707daced99a (MD5) Previous issue date: 2019Stanford Cardiovascular Institute. Stanford, CA, USA/Fundação Oswaldo Cruz. Instituto René Rachou. Belo Horizonte, MG, BrazilStanford Cardiovascular Institute. Stanford, CA, USA/Department of Medicine. Division of Cardiovascular Medicine. Stanford University. School of Medicine., Stanford, CA, USA/Department of Radiology. Stanford University. School of Medicine. Stanford, CA, USAStanford Cardiovascular Institute. Stanford, CA, USA/Department of Medicine. Division of Cardiovascular Medicine. Stanford University. School of Medicine., Stanford, CA, USA/Department of Radiology. Stanford University. School of Medicine. Stanford, CA, USADivision of Infectious Diseases and Geographic Medicine. Stanford University. School of Medicine, Stanford, CA, USA/California Institute for Medical Research. San Jose, CA, USAStanford Cardiovascular Institute. Stanford, CA, USA/Department of Medicine. Division of Cardiovascular Medicine. Stanford University. School of Medicine., Stanford, CA, USA/Department of Radiology. Stanford University. School of Medicine. Stanford, CA, USADivision of Infectious Diseases and Geographic Medicine. Stanford University. School of Medicine, Stanford, CA, USA/California Institute for Medical Research. San Jose, CA, USAFundação Oswaldo Cruz. Instituto René Rachou. Belo Horizonte, MG, BrazilDivision of Infectious Diseases and Geographic Medicine. Stanford University. School of Medicine, Stanford, CA, USA/California Institute for Medical Research. San Jose, CA, USAStanford Cardiovascular Institute. Stanford, CA, USA/Department of Medicine. Division of Cardiovascular Medicine. Stanford University. School of Medicine., Stanford, CA, USA/Department of Radiology. Stanford University. School of Medicine. Stanford, CA, USAChagas disease (ChD) is one of the most neglected tropical diseases, with cardiomyopathy being the main cause of death in Trypanosoma cruzi-infected patients. As the parasite actively replicates in cardiomyocytes (CMs), the heart remains a key target organ in the pathogenesis of ChD. Here we modeled ChD using human induced pluripotent stem cell-derived CMs (iPSC-CMs) to understand the complex interplay between the parasite and host cells. We showed that iPSC-CMs can get infected with the T. cruzi Y strain and that all parasite cycle stages can be identified in our model system. Importantly, characterization of T. cruzi-infected iPSC-CMs showed significant changes in their gene expression profile, cell contractility, and distribution of key cardiac markers. Moreover, these infected iPSC-CMs exhibited a pro-inflammatory profile as indicated by significantly elevated cytokine levels and cell-trafficking regulators. We believe our iPSC-CM model is a valuable platform to explore new treatment strategies for ChD