Efeito de várias disponibilidades hídricas, atuando como pré-condicionamento fisiológico durante a germinação das sementes de milho, no desenvolvimento das plântulas

The present paper considers the possible effects of physiological pre-treatment during the beginning of corn seeds germination in environments variable as to water availability (0 to -12 atm ). Periods of defficiency followed by 5 days without hydric limitations were compared with a control that remained equally, without reservations as to the disposability of water during 5 days. Results indicated that hydric pre-treatment of seeds can, if property adapted in its details, provide some advantages in the development of the seedlings derived from them. Chemical fungicide treatment of the seeds, submmited to the hydric pre-treatment may not be beneficial to the seedlings; as indicated by, in some isolated cases, the production of abnormalities in the embryonic structures.O presente trabalho buscou estimar os eventuais efeitos de pré-condicionamento fisiológico promovidos, durante o início da germinação das sementes de milho, por ambientes variáveis quanto à disponibilidade de água (0 a -12 atm). Para tanto, os períodos de deficiência eram sucedidos por prazos fixos de 5 dias sem limitações hídricas e comparados com uma testemunha que permaneceu, igualmente, sem restrições quanto à disponibilidade de água durante 5 dias. Os resultados encontrados indicaram que a técnica de pré-condicionamento hídrico das sementes pode, se devidamente adaptada em seus detalhes, propiciar algumas vantagens no desenvolvimento das plântulas delas oriundas. Adicionalmente, o tratamento químico fungicida das sementes, submetidas a pré-condicionamento hídrico, pode não trazer os benefícios esperados às plântulas; há casos isolados, ligados a produção de anormalidades nas estruturas embrionárias, em que o seu efeito é prejudicial

Genetic variation in PEAR1, cardiovascular outcomes and effects of aspirin in a healthy elderly population

This article is protected by copyright. All rights reserved. The platelet endothelial aggregation receptor-1 (PEAR1) rs12041331 variant has been identified as a genetic determinant of platelet aggregation in response to antiplatelet therapies, including aspirin. However, association with atherothrombotic cardiovascular events is less clear, with limited evidence from large trials. Here, we tested association of rs12041331 with cardiovascular events and aspirin use in a randomized trial population of healthy older individuals. We undertook post-hoc analysis of N=13,547 participants of the ASPirin in Reducing Events in the Elderly (ASPREE) trial, median age 74 years. Participants had no previous diagnosis of atherothrombotic cardiovascular disease at enrolment, and were randomized to either 100 mg daily low-dose aspirin or placebo for median 4.7 years follow-up. We used Cox proportional hazard regression to model the relationship between rs12041331 and the ASPREE primary cardiovascular disease endpoint (CVD), and composites of major adverse cardiovascular events (MACE) and ischaemic stroke (STROKE); and bleeding events; major hemorrhage (MHEM) and intracranial bleeding (ICB). We performed whole-population analysis using additive and dominant inheritance models, then stratified by treatment group. Interaction effects between genotypes and treatment group were examined. We observed no statistically significant association (P<0.05) in the population, or by treatment group, between rs12041331 and cardiovascular or bleeding events in either model. We also found no significant interaction effects between rs12041331-A and treatment group, for CVD (P=0.65), MACE (P=0.32), STROKE (P=0.56), MHEM (P=0.59) or ICB (P=0.56). The genetic variant PEAR1 rs12041331 is not associated with cardiovascular events in response to low-dose aspirin in a healthy elderly population

Levels and changes of HDL cholesterol and apolipoprotein A-I in relation to risk of cardiovascular events mmong statin-treated patients:a meta-analysis

It is unclear whether levels of high-density lipoprotein cholesterol (HDL-C) or apolipoprotein A-I (apoA-I) remain inversely associated with cardiovascular risk among patients who achieve very low levels of low-density lipoprotein cholesterol on statin therapy. It is also unknown whether a rise in HDL-C or apoA-I after initiation of statin therapy is associated with a reduced cardiovascular risk. We performed a meta-analysis of 8 statin trials in which lipids and apolipoproteins were determined in all study participants at baseline and at 1-year follow-up. Individual patient data were obtained for 38,153 trial participants allocated to statin therapy, of whom 5387 suffered a major cardiovascular event. HDL-C levels were associated with a reduced risk of major cardiovascular events (adjusted hazard ratio [HR], 0.83; 95% confidence interval [CI], 0.81-0.86 per 1 standard deviation increment), as were apoA-I levels (HR, 0.79; 95% CI, 0.72-0.82). This association was also observed among patients achieving on-statin low-density lipoprotein cholesterol levels <50 mg/dL. An increase of HDL-C was not associated with reduced cardiovascular risk (HR, 0.98; 95% CI, 0.94-1.01 per 1 standard deviation increment), whereas a rise in apoA-I was (HR, 0.93; 95% CI, 0.90-0.97). Among patients treated with statin therapy, HDL-C and apoA-I levels were strongly associated with a reduced cardiovascular risk, even among those achieving very low low-density lipoprotein cholesterol. An apoA-I increase was associated with a reduced risk of major cardiovascular events, whereas for HDL-C this was not the case. These findings suggest that therapies that increase apoA-I concentration require further exploration with regard to cardiovascular risk reductio