Morfologia, estrutura celular, metabolismo, nutrição e multiplicação de bactérias e leveduras

Unidade 2

Parâmetros urbanísticos na regulação do uso e ocupação do solo: estudo da densidade e do coeficiente de aproveitamento nos planos diretores de Natal de 1994 e 2007

A Constituição Federal de 1988 e o Estatuto da Cidade estabelecem o Plano Diretor como instrumento básico da política de ordenamento territorial, tendo como princípio fundamental o cumprimento da função social da propriedade e do direito à cidade. Na perspectiva de adequação às diretrizes e objetivos da política urbana estabelecidos em 1988, o município de Natal elaborou os Planos Diretores de 1994 e 2007, definindo instrumentos e parâmetros de regulação do uso e ocupação do solo possíveis de assegurar o cumprimento da função social da propriedade urbana e de gerar subsídios ao planejamento e à gestão da cidade. Apesar de Natal ter sido um dos municípios brasileiros pioneiros na adoção desses princ pios, antecipando e incorporando os instrumentos que em 2001 viriam a ser definidos no Estatuto da Cidade, identifica-se que alguns desses instrumentos e parâmetros direcionados à regulação do uso e ocupação do solo não tiveram sua aplicação plena, a exemplo do mecanismo de acompanhamento e controle dado pelo Estoque de Área Edificável e da Densidade, que foi substituída pelo Coeficiente de Aproveitamento no Plano Diretor de 2007. Questionando esse procedimento, busca-se na presente pesquisa investigar de que maneira essa substituição do parâmetro densidade pelo coeficiente de aproveitamento influenciou na capacidade da gestão pública de regular os processos de uso e ocupação do solo, de forma a adequar a sua intensificação ao suporte da infraestrutura instalada. Foram tomadas como referência teórico-conceitual as contribuições sobre a prática de planejamento urbano no Brasil, nos marcos do ideário da reforma urbana, com destaque para as reflexõe s de Flávio Villaça, Orlando Alves Santos Junior e Daniel Todtmann Montandon, Luiz César de Q. Ribeiro, Raquel Rolnik, Ermínia Maricato, Laura Machado de Bueno e Renato Cymbalista, José Roberto Bassul e Carlos F. Lago Burnett, e, com relação aos parâmetros de controle urbanístico, o estudo identifica as diferentes abordagens sobre a densidade urbana e o coeficiente de aproveitamento com base nas reflexões de Claudio Acioly Jr., Forbes Davidson, Juan Luis Mascaró, Ricardo Ojima, Marcelo de Souza, José Rámon Navarro Vera e Armando Ortuño Padilla, Nestor Goulart Reis, Marta Dora Grostein e Susana Ricardo Alves. Como conclusão, discute-se a hipótese formulada, inicialmente, de que a mudança de parâmetros verificada colocou limites para o município realizar uma gestão adequada do solo urbano e, portanto, de fazer cumprir a função social da propriedade, considerando a necessidade de adequação entre a intensificação do uso e ocupação do solo e a infraestrutura instalada

Papel da proteína de reparo XPC na regulação das proteínas de reparo APE1, OGG1 e PARP-1 em células humanas e de camundongos

studies using UV as a source of DNA damage. However, even though unrepaired UV-induced DNA damages are related to mutagenesis, cell death and tumorigenesis, they do not explain phenotypes such as neurodegeneration and internal tumors observed in patients with syndromes like Xeroderma Pigmentosum (XP) and Cockayne Syndrome (CS) that are associated with NER deficiency. Recent evidences point to a role of NER in the repair of 8-oxodG, a typical substrate of Base Excision Repair (BER). Since deficiencies in BER result in genomic instability, neurodegenerative diseases and cancer, it was investigated in this research the impact of XPC deficiency on BER functions in human cells. It was analyzed both the expression and the cellular localization of APE1, OGG1 e PARP-1, the mainly BER enzymes, in different NER-deficient human fibroblasts. The endogenous levels of these enzymes are reduced in XPC deficient cells. Surprisingly, XP-C fibroblasts were more resistant to oxidative agents than the other NER deficient fibroblasts, despite presenting the highest of 8-oxodG. Furthermore, subtle changes in the nuclear and mitochondrial localization of APE1 were detected in XP-C fibroblasts. To confirm the impact of XPC deficiency in the regulation of APE1 and OGG1 expression and activity, we constructed a XPC-complemented cell line. Although the XPC complementation was only partial, we found that XPC-complemented cells presented increased levels of OGG1 than XPC-deficient cells. The extracts from XPC-complemented cells also presented an elevated OGG1 enzimatic activity. However, it was not observed changes in APE1 expression and activity in the XPCcomplemented cells. In addition, we found that full-length APE1 (37 kDa) and OGG1- α are in the mitochondria of XPC-deficient fibroblasts and XPC-complemented fibroblasts before and after induction of oxidative stress. On the other hand, the expression of APE1 and PARP-1 are not altered in brain and liver of XPC knockout mice. However, XPC deficiency changed the APE1 localization in hypoccampus and hypothalamus. We also observed a physical interaction between XPC and APE1 proteins in human cells. In conclusion, the data suggest that XPC protein has a role in the regulation of OGG1 expression and activity in human cells and is involved mainly in the regulation of APE1 localization in mice. Aditionally, the response of NER deficient cells under oxidative stress may not be only associated to the NER deficiency per se, but it may include the new functions of NER enzymes in regulation of expression and cell localization of BER proteins

A infecção por Leishmania infantum chagasi altera o metabolismo lipídico do hospedeiro

American visceral leishmaniasis (AVL), caused by Leishmania infantum chagasi (L.i.chagasi), stands as a public health problem in Brazil, with human and canine cases related in all states..Lipid metabolism can be modified in several status of infection. For example, experimental studies show that the cholesterol is necessary to internalization and replication of L.i.chagasi in macrophages through caveolar domains. Patients with AVL present low levels of cholesterol and a visible triglycerides increase. This work aimed to evaluate the lipid metabolism in several post-infection status by L.i.chagasi, including individuals with symptomatic infection (AVL), and asymptomatic. The levels of cholesterol, triglycerides, HDL and reactive C protein, were measured. Individuals with AVL were compared with individuals with assymptomatic infection and presented low levels of total cholesterol (128 ± 6.180 mg/dL vs. 158 ±5.733 mg/dL, p=0.0001), HDL (29 ± 1.746 mg/dL vs. 37 ± 1.647 mg/dL, p=0.0001), increased levels of triglycerides (149.5 mg/dL ± 12.72 vs. 78.00 ± 10.43 mg/dL, p=0.0095) and higher levels of reactive C protein (1.750± 0.4939 mg/dL vs. 0.40 ± 0.1707 mg/dL; p=0.0001). The expression of genes related to lipid metabolism, such as LXR-a, LXR-b, PPAR-a, PPAR-d, PPAR-g and APOE was evaluated by real time PCR. A reduction in the expression of those genes was found in the group of AVL patients corroborating the serum levels of the metabolites earlier quantified. Our findings suggest a modulation of metabolism of lipids, in the chronic phase of AVL, this could facilitate the survival of leishmania, due to the known reduction on the ability of macrophages in presenting antigens efficiently to the T cells due to the reduction in the cholesterol available, it results in a subversion of the host immunity.