RESUMO Objetivou-se avaliar o efeito de diferentes doses de dois bioestimulantes sobre a produtividade e a estrutura do dossel do capim Urochloa brizantha cv. Marandu na fase de estabelecimento. O estudo foi realizado na Universidade Federal Rural da Amazônia, Parauapebas, Pará, Brasil. Um módulo de 35 parcelas de 25m² foi estabelecido. Utilizou-se delineamento experimental inteiramente ao acaso, composto de sete tratamentos e cinco repetições cada. Os tratamentos incluídos no controle foram: 0,5, 1 e 2kg/ha de bioestimulante A (BIOST.A); 0,25; 0,5 e 1L/ha de bioestimulante B (BIOST.B). Foram realizadas três coletas. Os dados para a aplicação dos dois bioestimulantes foram analisados separadamente, utilizando-se organização por método variável Dummy e análise de regressão. A aplicação de 2kg/ha BIOST.A resultou em incrementos de 842kg/ha na massa de forragem. A aplicação do BIOST.B na grama marandu resultou em aumento linear na produção de massa do caule. A aplicação de 2kg/ha BIOST.A no estabelecimento de erva de marandu resultou em maiores taxas de crescimento, acumulação de forragem e proporção de caule no dossel.

ABSTRACT The aim was to evaluate the effect of different doses of two biostimulants on the productivity and canopy structure of Urochloa brizantha cv. Marandu grass in the establishment fase. The study was conducted in Universidade Federal Rural da Amazônia, Parauapebas, Pará, Brazil. One module of 35 plots of 25m² were established. A completely randomized experimental design was used, with seven treatments and five replicates. The treatments included a control, 0.5, 1, and 2kg/ha of biostimulant A (BIOST.A); and 0.25, 0.5, and 1L/ha of biostimulant B (BIOST.B). Three collections were performed. The data for application of the two biostimulants were analyzed separately, using the Dummy variable method and regression analysis. The application of 2kg/ha BIOST.A resulted in increases of 842kg/ha in the forage mass. The application of BIOST.B on Marandu grass resulted in a linear increase in stem mass. The application of 2kg/ha BIOST.A in the establishment of Marandu grass result in higher growth rates, forage accumulation, and stem proportion in the canopy.

Gastric cancer is the forth most frequent malignancy and the second most common cause of cancer death worldwide. DNA methylation is the most studied epigenetic alteration, occurring through a methyl radical addition to the cytosine base adjacent to guanine. Many tumor genes are inactivated by DNA methylation in gastric cancer. We evaluated the DNA methylation status of ANAPC1, CDKN2A and TP53 by methylation-specific PCR in 20 diffuse- and 26 intestinal-type gastric cancer samples and 20 normal gastric mucosa in individuals from Northern Brazil. All gastric cancer samples were advanced stage adenocarcinomas. Gastric samples were surgically obtained at the João de Barros Barreto University Hospital, State of Pará, and were stored at -80°C before DNA extraction. Patients had never been submitted to chemotherapy or radiotherapy, nor did they have any other diagnosed cancer. None of the gastric cancer samples presented methylated DNA sequences for ANAPC1 and TP53. CDKN2A methylation was not detected in any normal gastric mucosa; however, the CDKN2A promoter was methylated in 30.4% of gastric cancer samples, with 35% methylation in diffuse-type and 26.9% in intestinal-type cancers. CDKN2A methylation was associated with the carcinogenesis process for ~30% diffuse-type and intestinal-type compared to non-neoplastic samples. Thus, ANAPC1 and TP53 methylation was probably not implicated in gastric carcinogenesis in our samples. CDKN2A can be implicated in the carcinogenesis process of only a subset of gastric neoplasias.

Gastric cancer is the second most frequent type of neoplasia and also the second most important cause of death in the world. Virtually all the established cell lines of gastric neoplasia were developed in Asian countries, and western countries have contributed very little to this area. In the present study we describe the establishment of the cell line ACP01 and characterize it cytogenetically by means of in vitro immortalization. Cells were transformed from an intestinal-type gastric adenocarcinoma (T4N2M0) originating from a 48-year-old male patient. This is the first gastric adenocarcinoma cell line established in Brazil. The most powerful application of the cell line ACP01 is in the assessment of cytotoxicity. Solid tumor cell lines from different origins have been treated with several conventional and investigational anticancer drugs. The ACP01 cell line is triploid, grows as a single, non-organized layer, similar to fibroblasts, with focus formation, heterogeneous division, and a cell cycle of approximately 40 h. Chromosome 8 trisomy, present in 60% of the cells, was the most frequent cytogenetic alteration. These data lead us to propose a multifactorial triggering of gastric cancer which evolves over multiple stages involving progressive genetic changes and clonal expansion.

Twelve breast fibroadenomas were analyzed cytogenetically and only four were found to have clonal alterations. The presence of chromosomal alterations in fibroadenomas must be the consequence of the proliferating process and must not be related to the etiology of this type of lesion. In contrast, the few fibroadenomas that exhibit chromosomal alterations are likely to be those presenting a risk of neoplastic transformation. Clonal numerical alterations involved chromosomes 8, 18, 19, and 21. Of the chromosomal alterations found in the present study, only monosomy of chromosomes 19 and 21 has been reported in breast fibroadenomas. The loss of chromosome 21 was the most frequent alteration found in our sample. The study of benign proliferations and their comparison with chromosome alterations in their malignant counterparts ought to result in a better understanding of the genes acting on cell proliferation alone, and of the genes that cause these cells to exhibit varied behaviors such as recurrences, spontaneous regression and fast growth.