Growth regulator losses from cotton plants due to rainfall

Plant growth regulators (PGRs) applied to cotton plants (Gossypium hirsutum L.) can be washed off by rainfall. It is expected that the closer the rainfall to spraying time, the higher the product loss and the higher the amount of product to be reapplied to reach the desired growth rate. The objective of this study was to evaluate the effects of time between rainfall and application of either mepiquat chloride or chlormequat chloride to cotton on plant growth, as well as, estimate the need for PGR reapplication. Cotton was grown in 12-L pots with soil in a greenhouse. PGRs were applied forty days after seedling emergence, when 50% of plants had one pinhead square. Rainfall was simulated 1, 2, 4, 6, or 24 h after spraying. Plant height was measured just before PGR application and then at 3-d intervals for 30 d. At harvest, the number of reproductive branches and structures were counted before dry matter phytomass determination. Both growth regulators reduced cotton dry matter yields regardless of rainfall interval. PGRs controlled excessive plant growth; however, their efficiency was reduced as the time elapsed until rainfall was shorter. Product losses were detected after all rainfall intervals, which, in field conditions would require PGR reapplication. Mepiquat chloride rates to be reapplied after rain were on average 17% higher than chlormequat chloride rates.Reguladores de crescimento aplicados às plantas de algodoeiro (Gossypium hirsutum L.) podem ser lavados em função da ocorrência de chuvas. Chuvas que ocorrem próximas à época de aplicação podem ocasionar elevada perda e necessidade de reaplicação dos produtos visando à taxa de crescimento desejada. Avaliou-se o efeito do intervalo de tempo entre a ocorrência de chuva simulada e a aplicação de cloreto de mepiquat e cloreto de chlormequat no algodoeiro no crescimento das plantas, além de estimar a necessidade de reaplicação dos reguladores. Plantas de algodão foram cultivadas em vasos de 12 L que permaneceram em casa de vegetação. Os reguladores de crescimento foram aplicados 40 dias após a emergência, quando 50% das plantas apresentavam botão floral. A chuva foi simulada 1, 2, 4, 6 e 24 horas após a aplicação dos reguladores. Determinou-se a altura das plantas antes da aplicação dos produtos e a cada 3 dias até o 30º dia. Na colheita, foi avaliado o número de ramos e estruturas reprodutivas, com posterior determinação da massa da matéria seca. Também foi determinado o crescimento acumulado e taxa de crescimento das plantas. Os dois reguladores reduziram a massa da matéria seca das plantas, independente do intervalo para ocorrência da chuva. O crescimento excessivo das plantas foi controlado, porém, com eficiência reduzida quanto menor o intervalo para simulação de chuva. Em todos os períodos avaliados houve perda de produtos, com necessidade de reaplicação. A taxa de reaplicação de cloreto de mepiquat para os diferentes intervalos de chuva foi, em média, 17% maior

Hdl levels and oxidizability during myocardial infarction are associated with reduced endothelial-mediated vasodilation and nitric oxide bioavailability

Acute phase response modifies high-density lipoprotein (HDL) into a dysfunctional particle that may favor oxidative/inflammatory stress and eNOS dysfunction. The present study investigated the impact of this phenomenon on patients presenting ST-elevation myocardial infarction (STEMI). Plasma was obtained from 180 consecutive patients within the first 24-h of onset of STEMI symptoms (D1) and after 5 days (D5). Nitrate/nitrite (NOx) and lipoproteins were isolated by gradient ultracentrifugation. The oxidizability of low-density lipoprotein incubated with HDL (HDLaoxLDL) and the HDL self-oxidizability (HDLautox) were measured after CuSO4 co-incubation. Anti-inflammatory activity of HDL was estimated by VCAM-1 secretion by human umbilical vein endothelial cells after incubation with TNF-α. Flow-mediated dilation (FMD) was assessed at the 30(th) day (D30) after STEMI. Among patients in the first tertile of admission HDL-Cholesterol (42 mg/dL) tertiles, respectively. From D1 to D5, there was a decrease in HDL size (-6.3 ± 0.3%; p 42 mg/dL) tertiles, respectively. From D1 to D5, there was a decrease in HDL size (-6.3 ± 0.3%; p < 0.001) and particle number (-22.0 ± 0.6%; p < 0.001) as well as an increase in both HDLaoxLDL (33%(23); p < 0.001) and HDLautox (65%(25); p < 0.001). VCAM-1 secretion after TNF-a stimulation was reduced after co-incubation with HDL from healthy volunteers (-24%(33); p = 0.009), from MI patients at D1 (-23%(37); p = 0.015) and at D30 (-22%(24); p = 0.042) but not at D5 (p = 0.28). During STEMI, high HDL-cholesterol is associated with a greater decline in endothelial function. In parallel, structural and functional changes in HDL occur reducing its anti-inflammatory and anti-oxidant properties237284084

Hdl Levels And Oxidizability During Myocardial Infarction Are Associated With Reduced Endothelial-mediated Vasodilation And Nitric Oxide Bioavailability

Objective: Acute phase response modifies high-density lipoprotein (HDL) into a dysfunctional particle that may favor oxidative/inflammatory stress and eNOS dysfunction. The present study investigated the impact of this phenomenon on patients presenting ST-elevation myocardial infarction (STEMI). Methods: Plasma was obtained from 180 consecutive patients within the first 24-h of onset of STEMI symptoms (D1) and after 5 days (D5). Nitrate/nitrite (NOx) and lipoproteins were isolated by gradient ultracentrifugation. The oxidizability of low-density lipoprotein incubated with HDL (HDLaoxLDL) and the HDL self-oxidizability (HDLautox) were measured after CuSO4 co-incubation. Anti-inflammatory activity of HDL was estimated by VCAM-1 secretion by human umbilical vein endothelial cells after incubation with TNF-α. Flow-mediated dilation (FMD) was assessed at the 30th day (D30) after STEMI. Results: Among patients in the first tertile of admission HDL-Cholesterol (&lt;33mg/dL), the increment of NOx from D1 to D5 [6.7(2; 13) vs. 3.2(-3; 10) vs. 3.5(-3; 12); p=0.001] and the FMD adjusted for multiple covariates [8.4(5; 11) vs 6.1(3; 10) vs. 5.2(3; 10); p=0.001] were higher than in those in the second (33-42mg/dL) or third (&gt;42mg/dL) tertiles, respectively. From D1 to D5, there was a decrease in HDL size (-6.3±0.3%; p&lt;0.001) and particle number (-22.0±0.6%; p&lt;0.001) as well as an increase in both HDLaoxLDL (33%(23); p&lt;0.001) and HDLautox (65%(25); p&lt;0.001). VCAM-1 secretion after TNF-a stimulation was reduced after co-incubation with HDL from healthy volunteers (-24%(33); p=0.009), from MI patients at D1 (-23%(37); p=0.015) and at D30 (-22%(24); p=0.042) but not at D5 (p=0.28). Conclusion: During STEMI, high HDL-cholesterol is associated with a greater decline in endothelial function. In parallel, structural and functional changes in HDL occur reducing its anti-inflammatory and anti-oxidant properties.2372840846Rader, D.J., Molecular regulation of HDL metabolism and function: implications for novel therapies (2006) J.Clin. Invest, 116 (12), pp. 3090-3100Kontush, A., Chapman, M.J., Antiatherogenic function of HDL particle subpopulations: focus on antioxidative activities (2010) Curr. Opin. Lipidol., 21 (4), pp. 312-318Besler, C., Heinrich, K., Rohrer, L., Doerries, C., Riwanto, M., Shih, D.M., Chroni, A., Landmesser, U., Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease (2011) J.Clin. Invest, 121 (7), pp. 2693-2708Gomaraschi, M., Ossoli, A., Favari, E., Adorni, M.P., Sinagra, G., Cattin, L., Veglia, F., Calabresi, L., Inflammation impairs eNOS activation by HDL in patients with acute coronary syndrome (2013) Cardiovasc Res., 100 (1), pp. 36-43Zheng, L., Nukuna, B., Brennan, M.L., Sun, M., Goormastic, M., Settle, M., Schmitt, D., Hazen, S.L., Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease (2004) J.Clin. Invest, 114 (4), pp. 529-541Artl, A., Marsche, G., Lestavel, S., Sattler, W., Malle, E., Role of serum amyloid A during metabolism of acute-phase HDL by macrophages (2000) Arterioscler. Thromb. Vasc. Biol., 20 (3), pp. 763-772Kontush, A., Chapman, M.J., Functionally defective high-density lipoprotein: a new therapeutic target at the crossroads of dyslipidemia, inflammation, and atherosclerosis (2006) Pharmacol. Rev., 58 (3), pp. 342-374Flammer, A.J., Anderson, T., Celermajer, D.S., Creager, M.A., Deanfield, J., Ganz, P., Hamburg, N.M., Lerman, A., The assessment of endothelial function: from research into clinical practice (2012) Circulation, 126 (6), pp. 753-767Quinaglia e Silva, J.C., Munhoz, D.B., Morato, T.N., Gurgel, A., Macedo, A.C., Sever, P., Sposito, A.C., Effect of beta blockers (metoprolol or propranolol) on effect of simvastatin in lowering C-reactive protein in acute myocardial infarction (2009) Am. J. Cardiol., 103 (4), pp. 461-463. , Brasilia Heart Study GChapman, M.J., Goldstein, S., Lagrange, D., Laplaud, P.M., Adensity gradient ultracentrifugal procedure for the isolation of the major lipoprotein classes from human serum (1981) J.Lipid Res., 22 (2), pp. 339-358Huang, J.M., Huang, Z.X., Zhu, W., Mechanism of high-density lipoprotein subfractions inhibiting copper-catalyzed oxidation of low-density lipoprotein (1998) Clin. 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Elevated Cetp Activity During Acute Phase Of Myocardial Infarction Is Independently Associated With Endothelial Dysfunction And Adverse Clinical Outcome

Objective: Recent data suggests that cholesteryl ester transfer protein (CETP) activity may interact with acute stress conditions via inflammatory-oxidative response and thrombogenesis. We investigated this assumption in patients with ST-elevation myocardial infarction (STEMI). Methods: Consecutive patients with STEMI (n=116) were enrolled &lt;24-hof symptoms onset and were followed for 180 days. Plasma levels of C-reactive protein (CRP), interleukin-2 (IL-2), tumor necrosis factor (TNFα), 8-isoprostane, nitric oxide (NOx) and CETP activity were measured at enrollment (D1) and at fifth day (D5). Flow-mediated dilation (FMD) was assessed by ultrasound and coronary thrombus burden (CTB) was evaluated by angiography. Results: Neither baseline nor the change of CETP activity from D1 to D5 was associated with CRP, IL-2, TNFα, 8-isoprostane levels or CTB. The rise in NOx from D1 to D5 was inferior [3.5(-1; 10) vs. 5.5(-1; 12); p&lt;0.001] and FMD was lower [5.9(5.5) vs. 9.6(6.6); p=0.047] in patients with baseline CETP activity above the median value than in their counterparts. Oxidized HDL was measured by thiobarbituric acid reactive substances (TBARS) in isolated HDL particles and increased from D1 to D5, and remaining elevated at D30. The change in TBARS content in HDL was associated with CETP activity (r=0.72; p=0.014) and FMD (r=-0.61; p=0.046). High CETP activity at admission was associated with the incidence of sudden death and recurrent MI at 30 days (OR 12.8; 95% CI 1.25-132; p=0.032) and 180 days (OR 3.3; 95% CI 1.03-10.7; p=0.044). Conclusions: An enhanced CETP activity during acute phase of STEMI is independently associated with endothelial dysfunction and adverse clinical outcome.2372777783Cazita, P.M., Barbeiro, D.F., Moretti, A.I., Quintao, E.C., Soriano, F.G., Human cholesteryl ester transfer protein expression enhances the mouse survival rate in an experimental systemic inflammation model: a novel role for CETP (2008) Shock, 30 (5), pp. 590-595Deguchi, H., Fernandez, J.A., Griffin, J.H., Plasma cholesteryl ester transfer protein and blood coagulability (2007) Thromb. Haemost., 98 (6), pp. 1160-1164Grion, C.M., Cardoso, L.T., Perazolo, T.F., Garcia, A.S., Barbosa, D.S., Morimoto, H.K., Lipoproteins and CETP levels as risk factors for severe sepsis in hospitalized patients (2010) Eur. J. Clin. Investig., 40 (4), pp. 330-338Frangogiannis, N.G., Smith, C.W., Entman, M.L., The inflammatory response in myocardial infarction (2002) Cardiovasc. 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Commun., 303 (1), pp. 313-319Ohmura, H., Watanabe, Y., Hatsumi, C., Sato, H., Daida, H., Mokuno, H., Possible role of high susceptibility of high-density lipoprotein to lipid peroxidative modification and oxidized high-density lipoprotein in genesis of coronary artery spasm (1999) Atherosclerosis, 142 (1), pp. 179-184Besler, C., Heinrich, K., Rohrer, L., Doerries, C., Riwanto, M., Shih, D.M., Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease (2011) J.Clin. Investig., 121 (7), pp. 2693-2708Luscher, T.F., Taddei, S., Kaski, J.C., Jukema, J.W., Kallend, D., Munzel, T., Vascular effects and safety of dalcetrapib in patients with or at risk of coronary heart disease: the dal-VESSEL randomized clinical trial (2012) Eur. Heart J., 33 (7), pp. 857-865Ehara, S., Ueda, M., Naruko, T., Haze, K., Itoh, A., Otsuka, M., Elevated levels of oxidized low density lipoprotein show a positive relationship with the severity of acute coronary syndromes (2001) Circulation, 103 (15), pp. 1955-1960Norata, G.D., Ongari, M., Uboldi, P., Pellegatta, F., Catapano, A.L., Liver X receptor and retinoic X receptor agonists modulate the expression of genes involved in lipid metabolism in human endothelial cells (2005) Int. J. Mol. Med., 16 (4), pp. 717-722Ray, K.K., Ditmarsch, M., Kallend, D., Niesor, E.J., Suchankova, G., Upmanyu, R., The effect of cholesteryl ester transfer protein inhibition on lipids, lipoproteins, and markers of HDL function after an acute coronary syndrome: the dal-ACUTE randomized trial (2014) Eur. Heart J., 35 (27), pp. 1792-1800Gomaraschi, M., Ossoli, A., Favari, E., Adorni, M.P., Sinagra, G., Cattin, L., Inflammation impairs eNOS activation by HDL in patients with acute coronary syndrome (2013) Cardiovasc. Res., 100 (1), pp. 36-43Sposito, A.C., Santos, S.N., de Faria, E.C., Abdalla, D.S., da Silva, L.P., Soares, A.A., Timing and dose of statin therapy define its impact on inflammatory and endothelial responses during myocardial infarction (2011) Arterioscler. Thromb. Vasc. Biol., 31 (5), pp. 1240-1246Guazzi, M., Reina, G., Gripari, P., Tumminello, G., Vicenzi, M., Arena, R., Prognostic value of flow-mediated dilatation following myocardial infarction (2009) Int. J. Cardiol., 132 (1), pp. 45-50Karatzis, E.N., Ikonomidis, I., Vamvakou, G.D., Papaioannou, T.G., Protogerou, A.D., Andreadou, I., Long-term prognostic role of flow-mediated dilatation of the brachial artery after acute coronary syndromes without ST elevation (2006) Am. J. Cardiol., 98 (11), pp. 1424-142