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1.
CBE Life Sci Educ ; 21(1): ar8, 2022 03.
Artigo em Inglês | MEDLINE | ID: mdl-34978921

RESUMO

The course-based research experience (CRE) with its documented educational benefits is increasingly being implemented in science, technology, engineering, and mathematics education. This article reports on a study that was done over a period of 3 years to explicate the instructional processes involved in teaching an undergraduate CRE. One hundred and two instructors from the established and large multi-institutional SEA-PHAGES program were surveyed for their understanding of the aims and practices of CRE teaching. This was followed by large-scale feedback sessions with the cohort of instructors at the annual SEA Faculty Meeting and subsequently with a small focus group of expert CRE instructors. Using a qualitative content analysis approach, the survey data were analyzed for the aims of inquiry instruction and pedagogical practices used to achieve these goals. The results characterize CRE inquiry teaching as involving three instructional models: 1) being a scientist and generating data; 2) teaching procedural knowledge; and 3) fostering project ownership. Each of these models is explicated and visualized in terms of the specific pedagogical practices and their relationships. The models present a complex picture of the ways in which CRE instruction is conducted on a daily basis and can inform instructors and institutions new to CRE teaching.


Assuntos
Modelos Educacionais , Estudantes , Engenharia , Docentes , Humanos , Matemática , Ensino
2.
J Wildl Dis ; 56(3): 631-635, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-31917630

RESUMO

Reticuloendotheliosis viruses (REVs) are known to cause immunosuppressive and oncogenic disease that affects numerous avian species. Reticuloendotheliosis viruses are present worldwide and recently have been reported in South America with cases of infected commercial flocks in Argentina. We surveyed for the presence of REV in birds from a state in the northern region of Brazil using real-time PCR. We report here the presence of REV in Brazil, detected in Muscovy Ducks (Cairina moschata), Wild Turkeys (Meleagris gallopavo), and chickens (Gallus gallus) at a relatively high prevalence (16.8%). Phylogenetic analysis indicated a close relationship of these strains to variants in the US. This study provides evidence of REV in the Amazon biome and provides a baseline for future surveillance of the virus in the region and throughout Brazil.


Assuntos
Galinhas , Patos , Vírus da Reticuloendoteliose Aviária/isolamento & purificação , Reticuloendoteliose Aviária/virologia , Perus , Animais , Brasil/epidemiologia , Variação Genética , Filogenia , Vírus da Reticuloendoteliose Aviária/genética , Reticuloendoteliose Aviária/epidemiologia
3.
Viruses ; 3(10): 1815-35, 2011 10.
Artigo em Inglês | MEDLINE | ID: mdl-22069517

RESUMO

Human T-cell leukemia virus type-1 (HTLV-1) is the etiological agent of adult T-cell leukemia (ATL), an aggressive and highly chemoresistant malignancy. Rho family GTPases regulate multiple signaling pathways in tumorigenesis: cytoskeletal organization, transcription, cell cycle progression, and cell proliferation. Geranylgeranylation of Rho family GTPases is essential for cell membrane localization and activation of these proteins. It is currently unknown whether HTLV-1-transformed cells are preferentially sensitive to geranylgeranylation inhibitors, such as GGTI-298. In this report, we demonstrate that GGTI-298 decreased cell viability and induced G(2)/M phase accumulation of HTLV-1-transformed cells, independent of p53 reactivation. HTLV-1-LTR transcriptional activity was inhibited and Tax protein levels decreased following treatment with GGTI-298. Furthermore, GGTI-298 decreased activation of NF-κB, a downstream target of Rho family GTPases. These studies suggest that protein geranylgeranylation contributes to dysregulation of cell survival pathways in HTLV-1-transformed cells.


Assuntos
Alquil e Aril Transferases/antagonistas & inibidores , Benzamidas/farmacologia , Vírus Linfotrópico T Tipo 1 Humano/fisiologia , Prenilação de Proteína/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Alquil e Aril Transferases/metabolismo , Ciclo Celular , Linhagem Celular Transformada , Sobrevivência Celular/efeitos dos fármacos , Transformação Celular Viral , Produtos do Gene tax/efeitos dos fármacos , Produtos do Gene tax/metabolismo , Vírus Linfotrópico T Tipo 1 Humano/efeitos dos fármacos , Humanos , Proteínas I-kappa B/metabolismo , Leucemia-Linfoma de Células T do Adulto/enzimologia , Leucemia-Linfoma de Células T do Adulto/virologia , NF-kappa B/antagonistas & inibidores , NF-kappa B/efeitos dos fármacos , NF-kappa B/metabolismo , Fosforilação , Transporte Proteico/efeitos dos fármacos , Proteína Supressora de Tumor p53/metabolismo
4.
J Virol ; 82(23): 11714-22, 2008 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-18799587

RESUMO

Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia. The transforming ability of Tax, the viral oncoprotein, is believed to depend on interactions with cell cycle regulators and on transactivation of genes that control cellular proliferation, including proliferating cell nuclear antigen (PCNA), a cofactor associated with DNA replication and repair. Tax associates with cellular transcription factors to alter their affinity for cognate DNA elements, leading to increased or decreased transcription from that promoter. Although it has been demonstrated that Tax transactivates the PCNA promoter, the mechanism of transcriptional activation is unknown. Here we report a cellular complex that binds specifically to a novel site within the minimal Tax-responsive element of the TATAA-less PCNA promoter. Mutation at this binding site or Tax expression inhibited complex formation and increased promoter activity, suggesting that the complex is a transcriptional repressor. The activation of PCNA gene expression by Tax and consequential decrease in nucleotide excision repair mediated by PCNA overexpression could contribute to the reduced DNA repair capacity and genomic instability observed in HTLV-1-infected cells.


Assuntos
Produtos do Gene tax/fisiologia , Antígeno Nuclear de Célula em Proliferação/genética , Ativação Transcricional , Linhagem Celular , Reparo do DNA , Humanos , Mutação , Regiões Promotoras Genéticas , Elementos de Resposta
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