Política de promoção da exportação : um olhar sobre a evolução da cultura de melão do Rio Grande do Norte

Some sectors in Brazil are earning notoriety in the international market, configuring itself in dynamic areas for the Country. The most typical case is the agribusiness. Rio Grande do Norte state has important role, because 90% of the output of the melon exported by Brazil is produced at Assu/Mossoró. The present work planned to verify the evolution of the culture of the melon produced at Assu/Mossoró area, from 1990 to 2003. Through descriptive research, utilizing the case study and documentary analysis of secondary data this work showed the evolution of the area reaped of melon in the pole Assu/Mossoró, the quantity produced of melon and of the value of the output of the melon between 1990 and 2003. The research verified that all of the factors studied show growth during the analyzed period, showing up the importance of the agribusiness for the region. However the analysis shows the vulnerability of the sector concerning external macroeconomics factors, such as the exchange rates. Showing the importance and/or dependence of the producers for public actions to development of the culture, that might be on areas like infrastructure, economics or taxes

Latim I : língua e cultura : Catulo : vida

Académico - Licenciaturas

Latim I : língua e cultura : Catulo : a paixão por Lésbia

Académico - Licenciaturas

Latim I : língua e cultura : Catulo : um poeta douto

Académico - Licenciaturas

Latim I : língua e cultura : Salústio : enquadramento histórico

Académico - Licenciaturas

Latim I : língua e cultura : Marcial : enquadramento histórico

Académico - Licenciatura

Latim I : língua e cultura : Marcial : poeta da sociedade I

Académico - Licenciaturas

Latim I : língua e cultura : Marcial : poeta da sociedade II

Académico - Licenciaturas

Latim I : língua e cultura : literatura latina : visão cronológica

Académico - Licenciaturas

BRS ARAGUAIA: híbrido de melão amarelo, produtivo e saboroso.

Equipe técnica: Valter Rodrigues Oliveira, Leonardo Silva Boiteux, Agnaldo Donizete Ferreira de Carvalho, Ailton Reis, André Nepomuceno Dusi, Carlos Alberto Lopes, Celso Luiz Moretti, Geni Livtin Villas Bôas, Ítalo Moraes Rocha Guedes, Jadir Borges Pinheiro, João Maria Charchar, Leonora Mansur Mattos, Mirtes Freitas de Lima, Ronessa Bartolomeu de Souza, Werito Fernandes de Melo, Gláucia Salles Cortopassi Buso, Marco Antônio Ferreira, Fernando Antonio de Souza Aragão, Francisco das Chagas Vidal Neto, Waldelice Oliveira de Paiva, João Ribeiro Crisóstomo, Ricardo Elesbão Alves, José Luiz Mosca, Heloisa Almeida Cunha Figueiras, Antônio Apoliano dos Santos, Nivaldo Duardo Costa (CPATSA), Joston Simão de Assis (CPATSA), Rita de Cássia Souza Dias (CPATSA), José Amauri Buso, Marcos Coelho.

Degradação da proteína Cry1Ac de Bacillus thuringiensis por bactérias de solo de cultura do algodão transgênico e convencional (Gossypium hirsutum).

2009

Aspectos toxicológicos e ambientais dos agrotóxicos aplicados na cultura do melão.

2008

Familial Systemic Mastocytosis With Germline Kit K509i Mutation Is Sensitive To Treatment With Imatinib, Dasatinib And Pkc412.

Mastocytosis are myeloproliferative neoplasms commonly related to gain-of-function mutations involving the tyrosine kinase domain of KIT. We herein report a case of familial systemic mastocytosis with the rare KIT K509I germ line mutation affecting two family members: mother and daughter. In vitro treatment with imatinib, dasatinib and PKC412 reduced cell viability of primary mast cells harboring KIT K509I mutation. However, imatinib was more effective in inducing apoptosis of neoplastic mast cells. Both patients with familial systemic mastocytosis had remarkable hematological and skin improvement after three months of imatinib treatment, suggesting that it may be an effective front line therapy for patients harboring KIT K509I mutation.

Ten-eleven-translocation 2 (tet2) Is Downregulated In Myelodysplastic Syndromes.

TET2, a member of the ten-eleven-translocation (TET) family genes that modify DNA by converting 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC), is located in chromosome 4q24 and is frequently mutated in myeloid malignancies. The impact of TET2 mutation on survival outcomes is still controversial; however, functional studies have proved that it is a loss-of-function mutation that impairs myeloid cell differentiation and contributes to the phenotype of myeloid neoplasia. We, herein, aimed to investigate TET2 expression in patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). A significantly decreased TET2 expression was observed in bone marrow cells from AML (n = 53) and patients with MDS (n = 64), compared to normal donors (n = 22). In MDS, TET2 expression was significantly reduced in RAEB-1/RAEB-2 compared to other WHO 2008 classifications, and a lower TET2 expression was observed at the time of MDS disease progression in four of five patients. In multivariate analysis, low TET2 expression (P = 0.03), male gender (P = 0.02), and WHO 2008 classification (P < 0.0001) were independent predictors of poorer overall survival. These results suggest that defective TET2 expression plays a role in the MDS pathophysiology and predicts survival outcomes in this disease.

Ankhd1 Silencing Inhibits Stathmin 1 Activity, Cell Proliferation And Migration Of Leukemia Cells.

ANKHD1 is highly expressed in human acute leukemia cells and potentially regulates multiple cellular functions through its ankyrin-repeat domains. In order to identify interaction partners of the ANKHD1 protein and its role in leukemia cells, we performed a yeast two-hybrid system screen and identified SIVA, a cellular protein known to be involved in proapoptotic signaling pathways. The interaction between ANKHD1 and SIVA was confirmed by co-imunoprecipitation assays. Using human leukemia cell models and lentivirus-mediated shRNA approaches, we showed that ANKHD1 and SIVA proteins have opposing effects. While it is known that SIVA silencing promotes Stathmin 1 activation, increased cell migration and xenograft tumor growth, we showed that ANKHD1 silencing leads to Stathmin 1 inactivation, reduced cell migration and xenograft tumor growth, likely through the inhibition of SIVA/Stathmin 1 association. In addition, we observed that ANKHD1 knockdown decreases cell proliferation, without modulating apoptosis of leukemia cells, while SIVA has a proapoptotic function in U937 cells, but does not modulate proliferation in vitro. Results indicate that ANKHD1 binds to SIVA and has an important role in inducing leukemia cell proliferation and migration via the Stathmin 1 pathway. ANKHD1 may be an oncogene and participate in the leukemia cell phenotype.