REGULADOR DE CRESCIMENTO NA PRODUTIVIDADE E QUALIDADE DE SEMENTES DE AVEIA-BRANCA

RESUMO A aveia-branca (Avena sativa) é uma importante alternativa para cultivos de inverno no sul do Brasil. Contudo, elevados percentuais de acamamento limitam sua produtividade. Nesse contexto, a utilização de reguladores de crescimento pode ser uma opção para evitar o acamamento e obter maior produtividade. O objetivo deste trabalho foi avaliar o efeito de doses do regulador de crescimento trinexapac-ethyl sobre as características agronômicas da aveia-branca, bem como sua influência na qualidade fisiológica e sanitária das sementes. Um experimento foi conduzido em campo, onde foi avaliada a influência de quatro doses de trinexapac-ethyl (0, 50, 100 e 150 g i.a. ha-1) sobre a estatura de planta, o diâmetro de colmo, o percentual de acamamento e os componentes do rendimento. Um segundo experimento foi conduzido em laboratório, onde sementes provenientes do estudo em campo foram avaliadas quanto a qualidade fisiológica a partir da mensuração da germinação, primeira contagem da germinação, condutividade elétrica, comprimento e massa de plântulas, envelhecimento acelerado, teste de frio, índice de velocidade de germinação, índice de velocidade de emergência, massa seca de plântulas em campo e sanidade pelo método de Blotter Test. A utilização de doses crescentes de trinexapac-ethyl reduziu de forma quadrática a estatura, bem como o acamamento de plantas de aveia-branca. A dose de 100 g i.a ha-1 de regulador de crescimento proporcionou os melhores resultados para os componentes de produtividade em A. sativa. O uso do trinexapac-ethyl afeta negativamente a germinação e o vigor de sementes de aveiabranca, assim como a sua sanidade, reduzindo a capacidade de estabelecimento e desenvolvimento inicial da cultura.

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Effect of trolox C on cardiac contracture induced by hydrogen peroxide

Hydrogen peroxide (H2O2) perfused into the aorta of the isolated rat heart induces a positive inotropic effect, with cardiac arrhythmia such as extrasystolic potentiation or cardiac contractures, depending on the dose. The last effect is similar to the "stone heart" observed in reperfusion injury and may be ascribed to lipoperoxidation (LPO) of the membrane lipids, to protein damage, to reduction of the ATP level, to enzymatic alterations and to cardioactive compounds liberated by LPO. These effects may result in calcium overload of the cardiac fibers and contracture ("stone heart"). Hearts from male Wistar rats (300-350 g) were perfused at 31oC with Tyrode, 0.2 mM trolox C, 256 mM H2O2 or trolox C + H2O2. Cardiac contractures (baseline elevation of the myograms obtained) were observed when hearts were perfused with H2O2 (Tyrode: 5.9 ± 3.2; H2O2: 60.5 ± 13.9% of the initial value); perfusion with H2O2 increased the LPO of rat heart homogenates measured by chemiluminescence (Tyrode: 3,199 ± 259; H2O2: 5,304 ± 133 cps mg protein-1 60 min-1), oxygen uptake (Tyrode: 0.44 ± 0.1; H2O2: 3.2 ± 0.8 nmol min-1 mg protein-1) and malonaldehyde (TBARS) formation (Tyrode: 0.12 ± 0; H2O2: 0.37 ± 0.1 nmol/ml). Previous perfusion with 0.2 mM trolox C reduced the LPO (chemiluminescence: 4,098 ± 531), oxygen uptake (0.51 ± 0) and TBARS (0.13 ± 0) but did not prevent the H2O2-induced contractures (33.3 ± 16%). ATP (Tyrode: 2.84 ± 0; H2O2: 0.57 ± 0) and glycogen levels (Tyrode: 0.46 ± 0; H2O2: 0.26 ± 0) were reduced by H2O2. Trolox did not prevent these effects (ATP: 0.84 ± 0 and glycogen: 0.27 ± 0). Trolox C is known to be more effective than a -tocopherol or g -tocopherol in reducing LPO though it lacks the phytol portion of vitamin E to be fixed to the cell membranes. Trolox C, unlike vitamin A, did not prevent the glycogen reduction induced by H2O2. Trolox C induced a positive chronotropic effect that resulted in higher energy consumption. The reduction of energy level seemed to be more important than LPO in the mechanism of H2O2-induced contracture

The time series convergence of dispersion in financial analysts' forecasts

Finansanalytiker har en stor betydelse för finansmarknaderna, speciellt igenom att förmedla information genom resultatprognoser. Typiskt är att analytiker i viss grad är oeniga i sina resultatprognoser, och det är just denna oenighet analytiker emellan som denna avhandling studerar. Då ett företag rapporterar förluster tenderar oenigheten gällande ett företags framtid att öka. På ett intuitivt plan är det lätt att tolka detta som ökad osäkerhet. Det är även detta man finner då man studerar analytikerrapporter - analytiker ser ut att bli mer osäkra då företag börjar gå med förlust, och det är precis då som även oenigheten mellan analytikerna ökar. De matematisk-teoretiska modeller som beskriver analytikers beslutsprocesser har däremot en motsatt konsekvens - en ökad oenighet analytiker emellan kan endast uppkomma ifall analytikerna blir säkrare på ett individuellt plan, där den drivande kraften är asymmetrisk information. Denna avhandling löser motsägelsen mellan ökad säkerhet/osäkerhet som drivkraft bakom spridningen i analytikerprognoser. Genom att beakta mängden publik information som blir tillgänglig via resultatrapporter är det inte möjligt för modellerna för analytikers beslutsprocesser att ge upphov till de nivåer av prognosspridning som kan observeras i data. Slutsatsen blir därmed att de underliggande teoretiska modellerna för prognosspridning är delvis bristande och att spridning i prognoser istället mer troligt följer av en ökad osäkerhet bland analytikerna, i enlighet med vad analytiker de facto nämner i sina rapporter. Resultaten är viktiga eftersom en förståelse av osäkerhet runt t.ex. resultatrapportering bidrar till en allmän förståelse för resultatrapporteringsmiljön som i sin tur är av ytterst stor betydelse för prisbildning på finansmarknader. Vidare används typiskt ökad prognosspridning som en indikation på ökad informationsasymmetri i redovisningsforskning, ett fenomen som denna avhandling därmed ifrågasätter.

Oxidative stress in the latissimus dorsi muscle of diabetic rats

The purpose of the present study was to investigate the effects of experimental diabetes on the oxidant and antioxidant status of latissimus dorsi (LD) muscles of male Wistar rats (220 ± 5 g, N = 11). Short-term (5 days) diabetes was induced by a single injection of streptozotocin (STZ, 50 mg/kg, iv; glycemia >300 mg/dl). LD muscle of STZ-diabetic rats presented higher levels of thiobarbituric acid reactive substances (TBARS) and chemiluminescence (0.36 ± 0.02 nmol/mg protein and 14706 ± 1581 cps/mg protein) than LD muscle of normal rats (0.23 ± 0.04 nmol/mg protein and 7389 ± 1355 cps/mg protein). Diabetes induced a 92% increase in catalase and a 27% increase in glutathione S-transferase activities in LD muscle. Glutathione peroxidase activity was reduced (58%) in STZ-diabetic rats and superoxide dismutase activity was similar in LD muscle of both groups. A positive correlation was obtained between catalase activity and the oxidative stress of LD, as evaluated in terms of TBARS (r = 0.78) and by chemiluminescence (r = 0.89). Catalase activity also correlated inversely with glutathione peroxidase activity (r = 0.79). These data suggest that an increased oxidative stress in LD muscle of diabetic rats may be related to skeletal muscle myopathy.

Myocardial antioxidant and oxidative stress changes due to sex hormones

The purpose of the present study was to examine myocardial antioxidant and oxidative stress changes in male and female rats in the presence of physiological sex hormone concentrations and after castration. Twenty-four 9-week-old Wistar rats were divided into four groups of 6 animals each: 1) sham-operated females, 2) castrated females, 3) sham-operated males, and 4) castrated males. When testosterone and estrogen levels were measured by radioimmunoassay, significant differences were observed between the castrated and control groups (both males and females), demonstrating the success of castration. Progesterone and catalase levels did not change in any group. Control male rats had higher levels of glutathione peroxidase (50%) and lower levels of superoxide dismutase (SOD, 14%) than females. Control females presented increased levels of SOD as compared to the other groups. After castration, SOD activity decreased by 29% in the female group and by 14% in the male group as compared to their respective controls. Lipid peroxidation (LPO) was assessed to evaluate oxidative damage to cardiac membranes by two different methods, i.e., TBARS and chemiluminescence. LPO was higher in male controls compared to female controls when evaluated by both methods, TBARS (360%) and chemiluminescence (46%). Castration induced a 200% increase in myocardial damage in females as determined by TBARS and a 20% increase as determined by chemiluminescence. In males, castration did not change LPO levels. These data suggest that estrogen may have an antioxidant role in heart muscle, while testosterone does not.

Lipid peroxidation and total radical-trapping potential of the lungs of rats submitted to chronic and sub-chronic stress

Exposure to stress induces a cluster of physiological and behavioral changes in an effort to maintain the homeostasis of the organism. Long-term exposure to stress, however, has detrimental effects on several cell functions such as the impairment of antioxidant defenses leading to oxidative damage. Oxidative stress is a central feature of many diseases. The lungs are particularly susceptible to lesions by free radicals and pulmonary antioxidant defenses are extensively distributed and include both enzymatic and non-enzymatic systems. The aim of the present study was to determine lipid peroxidation and total radical-trapping potential (TRAP) changes in lungs of rats submitted to different models of chronic stress. Adult male Wistar rats weighing 180-230 g were submitted to different stressors (variable stress, N = 7) or repeated restraint stress for 15 (N = 10) or 40 days (N = 6) and compared to control groups (N = 10 each). Lipid peroxidation levels were assessed by thiobarbituric acid reactive substances (TBARS), and TRAP was measured by the decrease in luminescence using the 2-2'-azo-bis(2-amidinopropane)-luminol system. Chronic variable stress induced a 51% increase in oxidative stress in lungs (control group: 0.037 ± 0.002; variable stress: 0.056 ± 0.007, P < 0.01). No difference in TBARS was observed after chronic restraint stress, but a significant 57% increase in TRAP was presented by the group repeatedly restrained for 15 days (control group: 2.48 ± 0.42; stressed: 3.65 ± 0.16, P < 0.05). We conclude that different stressors induce different effects on the oxidative status of the organism.

Peripheral markers of oxidative stress in chronic mercuric chloride intoxication

The present study was designed to evaluate the time course changes in peripheral markers of oxidative stress in a chronic HgCl2 intoxication model. Twenty male adult Wistar rats were treated subcutaneously daily for 30 days and divided into two groups of 10 animals each: Hg, which received HgCl2 (0.16 mg kg-1 day-1), and control, receiving the same volume of saline solution. Blood was collected at the first, second and fourth weeks of Hg administration to evaluate lipid peroxidation (LPO), total radical trapping antioxidant potential (TRAP), and superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and catalase (CAT). HgCl2 administration induced a rise (by 26%) in LPO compared to control (143 ± 10 cps/mg hemoglobin) in the second week and no difference was found at the end of the treatment. At that time, GST and GPx were higher (14 and 24%, respectively) in the Hg group, and Cu,Zn-SOD was lower (54%) compared to control. At the end of the treatment, Cu,Zn-SOD and CAT were higher (43 and 10%, respectively) in the Hg group compared to control (4.6 ± 0.3 U/mg protein; 37 ± 0.9 pmol/mg protein, respectively). TRAP was lower (69%) in the first week compared to control (43.8 ± 1.9 mM Trolox). These data provide evidence that HgCl2 administration is accompanied by systemic oxidative damage in the initial phase of the process, which leads to adaptive changes in the antioxidant reserve, thus decreasing the oxidative injury at the end of 30 days of HgCl2 administration. These results suggest that a preventive treatment with antioxidants would help to avoid oxidative damage in subjects with chronic intoxication.

The role of adrenergic receptor polymorphisms in heart failure

The main function of the cardiac adrenergic system is to regulate cardiac work both in physiologic and pathologic states. A better understanding of this system has permitted the elucidation of its role in the development and progression of heart failure. Regardless of the initial insult, depressed cardiac output results in sympathetic activation. Adrenergic receptors provide a limiting step to this activation and their sustained recruitment in chronic heart failure has proven to be deleterious to the failing heart. This concept has been confirmed by examining the effect of ß-blockers on the progression of heart failure. Studies of adrenergic receptor polymorphisms have recently focused on their impact on the adrenergic system regarding its adaptive mechanisms, susceptibilities and pharmacological responses. In this article, we review the function of the adrenergic system and its maladaptive responses in heart failure. Next, we discuss major adrenergic receptor polymorphisms and their consequences for heart failure risk, progression and prognosis. Finally, we discuss possible therapeutic implications resulting from the understanding of polymorphisms and the identification of individual genetic characteristics.

Hemodialysis improves endothelial venous function in end-stage renal disease

The objective of the present study was to determine the acute effect of hemodialysis on endothelial venous function and oxidative stress. We studied 9 patients with end-stage renal disease (ESRD), 36.8 ± 3.0 years old, arterial pressure 133.8 ± 6.8/80.0 ± 5.0 mmHg, time on dialysis 55.0 ± 16.6 months, immediately before and after a hemodialysis session, and 10 healthy controls matched for age and gender. Endothelial function was assessed by the dorsal hand vein technique using graded local infusion of acetylcholine (endothelium-dependent venodilation, EDV) and sodium nitroprusside (endothelium-independent venodilation). Oxidative stress was evaluated by measuring protein oxidative damage (carbonyls) and antioxidant defense (total radical trapping antioxidant potential - TRAP) in blood samples. All patients were receiving recombinant human erythropoietin for at least 3 months and were not taking nitrates or a-receptor antagonists. EDV was significantly lower in ESRD patients before hemodialysis (65.6 ± 10.5) vs controls (109.6 ± 10.8; P = 0.010) and after hemodialysis (106.6 ± 15.7; P = 0.045). Endothelium-independent venodilation was similar in all comparisons performed. The hemodialysis session significantly decreased TRAP (402.0 ± 53.5 vs 157.1 ± 28.3 U Trolox/µL plasma; P = 0.001). There was no difference in protein damage comparing ESRD patients before and after hemodialysis. The magnitude of change in the EDV was correlated negatively with the magnitude of change in TRAP (r = -0.70; P = 0.037). These results suggest that a hemodialysis session improves endothelial venous function, in association with an antioxidant effect.

The search for circadian clock components in humans: new perspectives for association studies

Individual circadian clocks entrain differently to environmental cycles (zeitgebers, e.g., light and darkness), earlier or later within the day, leading to different chronotypes. In human populations, the distribution of chronotypes forms a bell-shaped curve, with the extreme early and late types _ larks and owls, respectively _ at its ends. Human chronotype, which can be assessed by the timing of an individual's sleep-wake cycle, is partly influenced by genetic factors - known from animal experimentation. Here, we review population genetic studies which have used a questionnaire probing individual daily timing preference for associations with polymorphisms in clock genes. We discuss their inherent limitations and suggest an alternative approach combining a short questionnaire (Munich ChronoType Questionnaire, MCTQ), which assesses chronotype in a quantitative manner, with a genome-wide analysis (GWA). The advantages of these methods in comparison to assessing time-of-day preferences and single nucleotide polymorphism genotyping are discussed. In the future, global studies of chronotype using the MCTQ and GWA may also contribute to understanding the influence of seasons, latitude (e.g., different photoperiods), and climate on allele frequencies and chronotype distribution in different populations.

Acute exercise performed close to the anaerobic threshold improves cognitive performance in elderly females

The objective of the present study was to compare the effect of acute exercise performed at different intensities in relation to the anaerobic threshold (AT) on abilities requiring control of executive functions or alertness in physically active elderly females. Forty-eight physically active elderly females (63.8 ± 4.6 years old) were assigned to one of four groups by drawing lots: control group without exercise or trial groups with exercise performed at 60, 90, or 110% of AT (watts) and submitted to 5 cognitive tests before and after exercise. Following cognitive pretesting, an incremental cycle ergometer test was conducted to determine AT using a fixed blood lactate concentration of 3.5 mmol/L as cutoff. Acute exercise executed at 90% of AT resulted in significant (P < 0.05, ANOVA) improvement in the performance of executive functions when compared to control in 3 of 5 tests (verbal fluency, Tower of Hanoi test (number of movements), and Trail Making test B). Exercising at 60% of AT did not improve results of any tests for executive functions, whereas exercise executed at 110% of AT only improved the performance in one of these tests (verbal fluency) compared to control. Women from all trial groups exhibited a remarkable reduction in the Simple Response Time (alertness) test (P = 0.001). Thus, physical exercise performed close to AT is more effective to improve cognitive processing of older women even if conducted acutely, and using a customized exercise prescription based on the anaerobic threshold should optimize the beneficial effects.

Fine-tuning of defensive behaviors in the dorsal periaqueductal gray by atypical neurotransmitters

This paper presents an up-to-date review of the evidence indicating that atypical neurotransmitters such as nitric oxide (NO) and endocannabinoids (eCBs) play an important role in the regulation of aversive responses in the periaqueductal gray (PAG). Among the results supporting this role, several studies have shown that inhibitors of neuronal NO synthase or cannabinoid receptor type 1 (CB1) receptor agonists cause clear anxiolytic responses when injected into this region. The nitrergic and eCB systems can regulate the activity of classical neurotransmitters such as glutamate and γ-aminobutyric acid (GABA) that control PAG activity. We propose that they exert a ‘fine-tuning’ regulatory control of defensive responses in this area. This control, however, is probably complex, which may explain the usually bell-shaped dose-response curves observed with drugs that act on NO- or CB1-mediated neurotransmission. Even if the mechanisms responsible for this complex interaction are still poorly understood, they are beginning to be recognized. For example, activation of transient receptor potential vanilloid type-1 channel (TRPV1) receptors by anandamide seems to counteract the anxiolytic effects induced by CB1 receptor activation caused by this compound. Further studies, however, are needed to identify other mechanisms responsible for this fine-tuning effect.

Pleiotropic effects of simvastatin in physically trained ovariectomized rats

This study tested the hypothesis that simvastatin treatment can improve cardiovascular and autonomic functions and membrane lipoperoxidation, with an increased effect when applied to physically trained ovariectomized rats. Ovariectomized rats were divided into sedentary, sedentary+simvastatin and trained+simvastatin groups (n = 8 each). Exercise training was performed on a treadmill for 8 weeks and simvastatin (5 mg/kg) was administered in the last 2 weeks. Blood pressure (BP) was recorded in conscious animals. Baroreflex sensitivity was evaluated by the tachycardic and bradycardic responses to BP changes. Cardiac vagal and sympathetic effects were determined using methylatropine and propranolol. Oxidative stress was evaluated based on heart and liver lipoperoxidation using the chemiluminescence method. The simvastatin-treated groups presented reduced body weight and mean BP (trained+simvastatin = 99 ± 2 and sedentary+simvastatin = 107 ± 2 mmHg) compared to the sedentary group (122 ± 1 mmHg). Furthermore, the trained group showed lower BP and heart rate compared to the other groups. Tachycardic and bradycardic responses were enhanced in both simvastatin-treated groups. The vagal effect was increased in the trained+simvastatin group and the sympathetic effect was decreased in the sedentary+simvastatin group. Hepatic lipoperoxidation was reduced in sedentary+simvastatin (≈21%) and trained+simvastatin groups (≈57%) compared to the sedentary group. Correlation analysis involving all animals demonstrated that cardiac lipoperoxidation was negatively related to the vagal effect (r = -0.7) and positively correlated to the sympathetic effect (r = 0.7). In conclusion, improvement in cardiovascular and autonomic functions associated with a reduction of lipoperoxidation with simvastatin treatment was increased in trained ovariectomized rats.