Crescimento e rendimento do milho e da braquiária em sistema consorciado com diferentes manejos de plantas daninhas

Objetivou-se, neste trabalho, avaliar o crescimento e o rendimento do milho e da braquiária em monocultivos e consorciados, com diferentes manejos das plantas daninhas. O experimento foi realizado em área de pastagem degradada, num Latossolo Vermelho-Amarelo distrófico. Os tratamentos foram arranjados em esquema fatorial 4 x 4 + 5, sendo o primeiro fator correspondente aos cultivares de milho (UFV M100, DKB 390, DKB 455 e DKB 789) em consórcio com Urochloa brizantha, combinados com os diferentes manejos de plantas daninhas - capinado; sem controle de plantas daninhas; atrazine (1,5 kg ha-1); e atrazine + nicosulfuron (1,5 kg ha-1 + 8 g ha-1) -, além dos monocultivos capinados de U. brizantha e dos quatro cultivares de milho. O delineamento experimental utilizado foi o de blocos casualizados com quatro repetições. Aos 30, 60, 90, 120 e 150 dias após o plantio (DAP), avaliou-se a matéria seca do milho e da braquiária; na última avaliação, determinou-se, também, o rendimento de grãos do milho. Os maiores acúmulos de matéria seca e rendimentos foram obtidos nos monocultivos da braquiária e do milho. No entanto, a aplicação de atrazine + nicosulfuron no consórcio proporcionou rendimento de grãos de milho similar ao obtido no monocultivo. Os efeitos dos manejos das plantas daninhas e dos cultivares de milho no crescimento da braquiária somente se manifestaram nas avaliações realizadas aos 90, 120 e 150 DAP. Os híbridos de milho mostraram-se mais competitivos com a braquiária do que a variedade; o maior rendimento de grãos foi obtido com o híbrido simples (DKB 390), e o menor, com o híbrido triplo (DKB 455). A interferência de U. brizantha no milho, quando cultivados em consórcio, depende das práticas de manejo de plantas daninhas e do cultivar de milho adotado

Female chromosome X mosaicism is age-related and preferentially affects the inactivated X chromosome

To investigate large structural clonal mosaicism of chromosome X, we analysed the SNP microarray intensity data of 38,303 women from cancer genome-wide association studies (20,878 cases and 17,425 controls) and detected 124 mosaic X events42Mb in 97 (0.25%) women. Here we show rates for X-chromosome mosaicism are four times higher than mean autosomal rates; X mosaic events more often include the entire chromosome and participants with X events more likely harbour autosomal mosaic events. X mosaicism frequency increases with age (0.11% in 50-year olds; 0.45% in 75-year olds), as reported for Y and autosomes. Methylation array analyses of 33 women with X mosaicism indicate events preferentially involve the inactive X chromosome. Our results provide further evidence that the sex chromosomes undergo mosaic events more frequently than autosomes, which could have implications for understanding the underlying mechanisms of mosaic events and their possible contribution to risk for chronic diseases

Detectable clonal mosaicism and its relationship to aging and cancer

In an analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies, we observed large chromosomal abnormalities in a subset of clones in DNA obtained from blood or buccal samples. We observed mosaic abnormalities, either aneuploidy or copy-neutral loss of heterozygosity, of >2 Mb in size in autosomes of 517 individuals (0.89%), with abnormal cell proportions of between 7% and 95%. In cancer-free individuals, frequency increased with age, from 0.23% under 50 years to 1.91% between 75 and 79 years (P = 4.8 × 10(-8)). Mosaic abnormalities were more frequent in individuals with solid tumors (0.97% versus 0.74% in cancer-free individuals; odds ratio (OR) = 1.25; P = 0.016), with stronger association with cases who had DNA collected before diagnosis or treatment (OR = 1.45; P = 0.0005). Detectable mosaicism was also more common in individuals for whom DNA was collected at least 1 year before diagnosis with leukemia compared to cancer-free individuals (OR = 35.4; P = 3.8 × 10(-11)). These findings underscore the time-dependent nature of somatic events in the etiology of cancer and potentially other late-onset diseases