Efficient time series detection of the strong stochasticity threshold in Fermi-Pasta-Ulam oscillator lattices

In this work we study the possibility of detecting the so-called strong stochasticity threshold, i.e. the transition between weak and strong chaos as the energy density of the system is increased, in anharmonic oscillator chains by means of the 0-1 test for chaos. We compare the result of the aforementioned methodology with the scaling behavior of the largest Lyapunov exponent computed by means of tangent space dynamics, that has so far been the most reliable method available to detect the strong stochasticity threshold. We find that indeed the 0-1 test can perform the detection in the range of energy density values studied. Furthermore, we determined that conventional nonlinear time series analysis methods fail to properly compute the largest Lyapounov exponent even for very large data sets, whereas the computational effort of the 0-1 test remains the same in the whole range of values of the energy density considered with moderate size time series. Therefore, our results show that, for a qualitative probing of phase space, the 0-1 test can be an effective tool if its limitations are properly taken into account.Comment: 5 pages, 2 figures; accepted for publication in Physical Review

The H+-ATP synthase: A gate to ROS-mediated cell death or cell survival

This article is part of a Special Issue entitled: 18th European Bioenergetic ConferenceCellular oxidative stress results from the increased generation of reactive oxygen species and/or the dysfunction of the antioxidant systems. Most intracellular reactive oxygen species derive from superoxide radical although the majority of the biological effects of reactive oxygen species are mediated by hydrogen peroxide. In this contribution we overview the major cellular sites of reactive oxygen species production, with special emphasis in the mitochondrial pathways. Reactive oxygen species regulate signaling pathways involved in promoting survival and cell death, proliferation, metabolic regulation, the activation of the antioxidant response, the control of iron metabolism and Ca2 + signaling. The reversible oxidation of cysteines in transducers of reactive oxygen species is the primary mechanism of regulation of the activity of these proteins. Next, we present the mitochondrial H+-ATP synthase as a core hub in energy and cell death regulation, defining both the rate of energy metabolism and the reactive oxygen species-mediated cell death in response to chemotherapy. Two main mechanisms that affect the expression and activity of the H+-ATP synthase down-regulate oxidative phosphorylation in prevalent human carcinomas. In this context, we emphasize the prominent role played by the ATPase Inhibitory Factor 1 in human carcinogenesis as an inhibitor of the H+-ATP synthase activity and a mediator of cell survival. The ATPase Inhibitory Factor 1 promotes metabolic rewiring to an enhanced aerobic glycolysis and the subsequent production of mitochondrial reactive oxygen species. The generated reactive oxygen species are able to reprogram the nucleus to support tumor development by arresting cell death. Overall, we discuss the cross-talk between reactive oxygen species signaling and mitochondrial function that is crucial in determining the cellular fateWork in the authors’ laboratory was supported by grants from the Ministerio de Educación y Ciencia (BFU2010-18903), by the Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), ISCIII and by Comunidad de Madrid (S/2011-BMD-2402), Spain. The CBMSO receives an institutional grant from Fundación Ramón Arece

Sobre condiciones de integrabilidad de una estructura j satisfaciendo (j2-p2) (j2 +q2 ) = 0

We consider the structures defined by a tensor field J of type (1,1) which satisfy the condition (J2-p2)(J2+q2)=0 characterizing its integrability in term of its Nijenhuis tenso

miR-127-5p targets the 3'UTR of human β-F1-ATPase mRNA and inhibits its translation

IMW and IMR are the recipients of pre-doctoral fellowships from the Plan de Formación de Profesorado Universitario (AP2007-03035) from the Ministerio de Educación and JAE-CSIC, respectively. The work was supported by grants from the Ministerio de Educación y Ciencia (BFU2010- 18903), by the Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), ISCIII and by Comunidad de Madrid (S2011/BMD-2402), Spain. The CBMSO receives an institutional grant from Fundación Ramón Arece

AMPK and GCN2-ATF4 signal the repression of mitochondria in colon cancer cells

Reprogramming of energetic metabolism is a phenotypic trait of cancer in which mitochondrial dysfunction represents a key event in tumour progression. In the present study, we show that the acquisition of the tumour-promoting phenotype in colon cancer HCT116 cells treated with oligomycin to inhibit ATP synthase is exerted by repression of the synthesis of nuclear-encoded mitochondrial proteins in a process that is regulated at the level of translation. Remarkably, the synthesis of glycolytic proteins is not affected in this situation. Changes in translational control of mitochondrial proteins are signalled by the activation of AMPK (AMP-activated protein kinase) and the GCN2 (general control non-derepressible 2) kinase, leading also to the activation of autophagy. Changes in the bioenergetic function of mitochondria are mimicked by the activation of AMPK and the silencing of ATF4 (activating transcription factor 4). These findings emphasize the relevance of translational control for normal mitochondrial function and for the progression of cancer. Moreover, they demonstrate that glycolysis and oxidative phosphorylation are controlled at different levels of gene expression, offering the cell a mechanistic safeguard strategy for metabolic adaptation under stressful conditions.</jats:p

Development of type 2 diabetes mellitus thirty-one years after Billroth II in a patient asking for diabetes surgery

Introduction: Diabetes surgery in obese and slim patients seems to be a superior alternative to the current medical treatment. Gastric bypass is an alternative treat- ment for diabetes. Nevertheless, there are still doubts whether diabetes can recur if you gain weight or if the effects are maintained over time. Other questions refer to the type of surgery to make the bypass limb length or reservoir size for the resolution of the Diabetes Mellitus. Presentation of case: Male patient 69-year-old came to us in order to perform tailored One Anastomosis Gastric Bypass (BAGUA) to treat his type 2 diabetes mellitus and metabolic syndrome. He has a history of peptic ulcer treated with subtotal gastrectomy and Billroth II recons- truction 49 years ago. He currently is not obese and deve- loped diabetes 31 years after surgery. Discussion: Globally there are no reports of patients with normal BMI that after performing gastric bypass developed diabetes mellitus. There are cases where obese diabetic patients after gastric bypass improve or remits the T2DM, but it relapses due to insufficient weight loss or gain it. The patient with gastric bypass Billroth II type, should not developed diabetes. He is normal weight and not had weight gain that could be linked to the develop- ment of diabetes. Conclusions: The results generated by bariatric surgery are encouraging, but still do not clarify the precise way how surgery produces rapid improvement of systemic metabolism as in diabetes, but in our patient, the effect was quite different because the gastric bypass had no protective effect against diabetes

A catalog of planetary nebula candidates in the Sculptor spiral galaxy NGC 300

[OIII]5007 on-band off-band images, obtained with the VLT and FORS2 spectrograph in two zones (center and outskirts) of the spiral galaxy NGC300, are analyzed searching for emission line objects. In particular we search for planetary nebula (PN) candidates to analyze their distribution and luminosity properties, to perform follow-up spectroscopy, and to study the planetary nebula luminosity function, PNLF. In the continuum-subtracted images, a large number of emission line objects were detected. From this sample we selected as PN candidates those objects with stellar appearance and no detectable central star. [OIII]5007 instrumental magnitudes were measured and calibrated by using spectrophotometric data from the follow-up spectroscopy. We identified more than a hundred PN candidates and a number of compact HII regions. The PN sample is the largest one reported for this galaxy so far. For all the objects we present coordinates, instrumental [OIII]5007 magnitudes and apparent nebular [OIII]5007 fluxes and magnitudes. The [OIII]5007 observed luminosity function for PNe (PNLF) was calculated for the whole sample and for the central and outskirts samples. The three PNLF are similar within uncertainties. We fit the empirical PNLF to the observed PNLF for all the samples. From our best fit for the whole sample we derived a maximum value for the apparent magnitudes of m*(5007)=22.019\pm0.022 and we obtained a tentative estimate of the distance modulus m(5007)-M(5007)= 26.29 {+0.12} {-0.22} mag, which agrees well with the recent value derived from Cepheid stars.Comment: 8 pages, 3 figures, one long table. Accepted by A&

Cancer Reduces Transcriptome Specialization

A central goal of cancer biology is to understand how cells from this family of genetic diseases undergo specific morphological and physiological changes and regress to a de-regulated state of the cell cycle. The fact that tumors are unable to perform most of the specific functions of the original tissue led us to hypothesize that the degree of specialization of the transcriptome of cancerous tissues must be less than their normal counterparts. With the aid of information theory tools, we analyzed four datasets derived from transcriptomes of normal and tumor tissues to quantitatively test the hypothesis that cancer reduces transcriptome specialization. Here, we show that the transcriptional specialization of a tumor is significantly less than the corresponding normal tissue and comparable with the specialization of dedifferentiated embryonic stem cells. Furthermore, we demonstrate that the drop in specialization in cancerous tissues is largely due to a decrease in expression of genes that are highly specific to the normal organ. This approach gives us a better understanding of carcinogenesis and offers new tools for the identification of genes that are highly influential in cancer progression