18 research outputs found
Effect of magnetic field on the fermentation kinetics of Saccharomyces cerevisiae
Published literature has shown conflicting results regarding the effects of magnetic fields on the fermentation kinetics or cellular growth of various Saccharomyces cerevisiae strains. Here, two sets of experiments were conducted to characterize the role of magnetic fields on cell growth and ethanol production during fermentation. The first experiment was completed for 25 h at a 2% dextrose loading rate under influence of homogeneous and non-homogeneous static magnetic fields on the order of 100 and 200 mT, respectively. The second experiment was completed for 30 h at a 6% dextrose loading rate under the influence of a non-homogeneous static magnetic field on the order of 200 mT. It was found that homogeneous magnetic fields have no significant effect on the yeast cell growth, while non-homogeneous static magnetic fields produced an increase (~ 8% over the control) in peak ethanol concentration with 2% dextrose loading. </p
Performance of the frontal and healthy control groups on the background measures and the parallel forms of the CET.
<p>NART = National Adult Reading Test; APM = Advanced Progressive Matrices; GNT = Graded Naming Test; GDA = Graded Difficulty Arithmetic.</p
Performance of the 184 healthy volunteers on the background neuropsychological measures.
<p>NART = National Adult Reading Test; APM = Advanced Progressive Matrices; GNT = Graded Naming Test; GDA = Graded Difficulty Arithmetic.</p
Distribution of the participants’ demographic characteristics according to age, education and gender.
<p>M = Male; F = Female.</p
Percentiles of the distribution of the adjusted error scores on the parallel versions of the CET.
<p>The possible scores range from zero (best performance) to 27 (worst performance).</p
Correlational analyses between CET performance and the background neuropsychological measures.
<p>NART = National Adult Reading Test; APM = Advanced Progressive Matrices; GNT = Graded Naming Test; GDA = Graded Difficulty Arithmetic.</p
Autophagic homeostasis is required for the pluripotency of cancer stem cells
<p>Pluripotency is an important feature of cancer stem cells (CSCs) that contributes to self-renewal and chemoresistance. The maintenance of pluripotency of CSCs under various pathophysiological conditions requires a complex interaction between various cellular pathways including those involved in homeostasis and energy metabolism. However, the exact mechanisms that maintain the CSC pluripotency remain poorly understood. In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD<sup>+</sup> synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1). First, our data show that the pharmacological inhibition and knockdown (K<sub>D</sub>) of NAMPT or the K<sub>D</sub> of POU5F1 in human CSCs significantly decreased the expression of pluripotency markers POU5F1, NANOG (Nanog homeobox) and SOX2 (SRY-box 2), and upregulated the differentiation markers TUBB3 (tubulin β 3 class III), CSN2 (casein β), SPP1 (secreted phosphoprotein 1), GATA6 (GATA binding protein 6), T (T brachyury transcription factor) and CDX2 (caudal type homeobox 2). Interestingly, these pluripotency-regulating effects of NAMPT and POU5F1 were accompanied by contrasting levels of autophagy, wherein NAMPT K<sub>D</sub> promoted while POU5F1 K<sub>D</sub> inhibited the autophagy machinery. Most importantly, any deviation from the basal level of autophagy, either increase (via rapamycin, serum starvation or Tat-beclin 1 [Tat-BECN1] peptide) or decrease (via ATG7 or ATG12 K<sub>D</sub>), strongly decreased the pluripotency and promoted the differentiation and/or senescence of CSCs. Collectively, these results uncover the link between the NAD<sup>+</sup> biosynthesis pathway, CSC transcription factor POU5F1 and pluripotency, and further identify autophagy as a novel regulator of pluripotency of CSCs.</p
