High intracellular trehalase activity prevents the storage of trehalose in the yeast Dekkera bruxellensis.

UNLABELLED: Dekkera bruxellensis hit the spotlight in the past decade mostly due to its rather high ability to adapt to several different fermentation processes. This yeast relies on different genetic and physiological aspects to achieve and preserve its high industrial fitness and some of these traits are shared with Saccharomyces cerevisiae. We have previously described that D. bruxellensis is unable to make use of accumulating trehalose as a strategy for cell adaptation and survival in the industrial scenario, as opposed to S. cerevisiae. Since trehalose is often involved in mechanisms related to cell protection, we aimed to investigate both cause and effect of the absence of this metabolite in the cell adaptive capacity in the industrial environment. Our results indicate that the major cause for the nonaccumulation of trehalose is the high constitutive activity of neutral trehalase. Therefore, the rate of trehalose degradation could be higher than its rate of synthesis, preventing accumulation. Altogether, our data elucidate the mechanisms involved in the lack of trehalose accumulation in D. bruxellensis as well as evaluates the implications of this feature. SIGNIFICANCE AND IMPACT OF THE STUDY: Dekkera bruxellensis can successfully take advantage of its peculiar physiological and genetic traits in order to adapt and survive in fermentation processes. So far, tolerance to stress has been credited to trehalose synthesis. The data presented in this work provided information on the underlying mechanism that prevents trehalose accumulation and corroborated the recent information that trehalose itself is not implicated in yeast stress tolerance. Second, it showed that D. bruxellensis responds differently to Saccharomyces cerevisiae to excess of sugar, which may explain its preference for respiration (oxidative metabolism) over fermentation (reductive metabolism) even at limited oxygen supply. These findings help to understand the drop on ethanol production in processes overtaken by this yeast.

Propranolol reduces myocardial hypertrophy in the right cardiac chambers after infarction in rats.

The effects of chronic propranolol (Prop) therapy on the postinfarction myocardial hypertrophy of infarcted rats were studied by histological techniques. Male albino rats were submitted to left coronary artery ligation to produce infarction or to sham surgery (Con, N = 6). Infarcted rats (Inf) were divided into 2 groups receiving Prop (2.5 mg/kg, twice a day, N = 6) or saline (N = 6) for one month, respectively. Myocyte diameters were measured in longitudinally oriented sections in the four heart chambers (60 cells/chamber). Inf produced a significant increase in mean diameter of myocytes from the right atrium and ventricle and from the left atrium. In the right ventricle, myocyte diameter increased from 8.9 +/- 0.5 microns in the Con group to 12.5 +/- 0.6 microns in the Inf group (P < 0.05). Under Prop, myocyte diameter was reduced (P < 0.05) to 9.8 +/- 0.9 microns. Similar values were observed in the right atrium. In the left atrium, Prop produced only a partial reversion of the postinfarction hypertrophy. In the left ventricle, myocyte diameter was not significantly changed after Inf or Prop therapy. These data show that beta blockers reduce the myocardial hypertrophy in the right heart chambers after experimental infarcts in rats. This effect can be secondary to reduction of pulmonary hypertension or to blockade of direct effects of catecholamines on myocardial fibers or both.

Propanolol reduces myocardial hypertrophy in the right cardiac chambers after infarction in rats

The effects of chronic propanolol (Prop) therapy on the post infarction myocardial hypertrophy of infarction rats were studied by histological techniques. male albino rats were submitted to left coronary artery ligation to produce infarction or to sham surgery (Con, N=6)., Infarction rats (Inf) were divided into 2 groups receiving Prop (2.5 mg/kg, twice a day, N+6) or saline (N=6) for one month, respectively. Myocyte diameters were measured in longitudinally oriented sections in the four heart chambers (60 cells/chamber). inf produced a significant increase in mean diameter of myocytes from the right atrium and ventricle and from the left atrium. In the right ventricle, myocyte diameter increased from 8.9 ñ 0.5 um in the Con group to 12.5 ñ 0.6 um in the the Inf group (P<0.05). Under Prop, myocyte diameter was reduced (P<0.05) to 9.8 ñ 0.9 um. Similar values were observed in the right atrium. In the left atrium, Prop produced only a partial reversion of the postinfarction hypertrophy. In the left ventricle, myocyte diameter was not significantly changed after Inf or Prop therapy. These data show that beta blockers reduce the myocardial hypertrophy in the right heart chambers after experimental infarcts in rats. This effect can be secondary to reduction of pulmonary hypertension or to blockade of direct effects of catecholamines on myocardial fibers or both