National Institute of Genomic Medicine

Tlalpan, Mexico

National Institute of Genomic Medicine

Tlalpan, Mexico
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Espinal-Enriquez J.,National Institute of Genomic Medicine | Espinal-Enriquez J.,Center for Complexity science | Larralde H.,National Autonomous University of Mexico
PLoS ONE | Year: 2015

Since December 2006, more than a thousand cities in México have suffered the effects of the war between several drug cartels, amongst themselves, as well as with Mexican armed forces. Sources are not in agreement about the number of casualties of this war, with reports varying from 30 to 100 thousand dead; the economic and social ravages are impossible to quantify. In this work we analyze the official report of casualties in terms of the location and the date of occurrence of the homicides. We show how the violence, as reflected by the number of casualties, has increased over time and spread across the country. Next, based on the correlations between cities in the changes of the monthly number of casualties attributed to organized crime, we construct a narco-war network where nodes are the affected cities and links represent correlations between them. We find that close geographical distance between violent cities does not imply a strong correlation amongst them. We observe that the dynamics of the conflict has evolved in short-term periods where a small core of violent cities determines the main theatre of the war at each stage. This kind of analysis may also help to describe the emergence and propagation of gang-related violence waves. © 2015 Espinal-Enríquez, Larralde. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Hernandez-Lemus E.,National Institute of Genomic Medicine
PloS one | Year: 2012

In the past, a great deal of attention has been drawn to thermal driven denaturation processes. In recent years, however, the discovery of stress-induced denaturation, observed at the one-molecule level, has revealed new insights into the complex phenomena involved in the thermo-mechanics of DNA function. Understanding the effect of local pressure variations in DNA stability is thus an appealing topic. Such processes as cellular stress, dehydration, and changes in the ionic strength of the medium could explain local pressure changes that will affect the molecular mechanics of DNA and hence its stability. In this work, a theory that accounts for hysteresis in pressure-driven DNA denaturation is proposed. We here combine an irreversible thermodynamic approach with an equation of state based on the Poisson-Boltzmann cell model. The latter one provides a good description of the osmotic pressure over a wide range of DNA concentrations. The resulting theoretical framework predicts, in general, the process of denaturation and, in particular, hysteresis curves for a DNA sequence in terms of system parameters such as salt concentration, density of DNA molecules and temperature in addition to structural and configurational states of DNA. Furthermore, this formalism can be naturally extended to more complex situations, for example, in cases where the host medium is made up of asymmetric salts or in the description of the (helical-like) charge distribution along the DNA molecule. Moreover, since this study incorporates the effect of pressure through a thermodynamic analysis, much of what is known from temperature-driven experiments will shed light on the pressure-induced melting issue.

Rangel-Vega A.,National Autonomous University of Mexico | Bernstein L.R.,TerrametrixCA | Mandujano-Tinoco E.A.,National Institute of Genomic Medicine | Garcia-Contreras S.J.,Centro Medico Coyoacan | Garcia-Contreras R.,National Autonomous University of Mexico
Frontiers in Microbiology | Year: 2015

Bacterial infection remains one of the leading causes of death worldwide, and the options for treating such infections are decreasing, due the rise of antibiotic-resistant bacteria. The pharmaceutical industry has produced few new types of antibiotics in more than a decade. Researchers are taking several approaches toward developing new classes of antibiotics, including (1) focusing on new targets and processes, such as bacterial cell-cell communication that upregulates virulence; (2) designing inhibitors of bacterial resistance, such as blockers of multidrug efflux pumps; and (3) using alternative antimicrobials such as bacteriophages. In addition, the strategy of finding new uses for existing drugs is beginning to produce results: antibacterial properties have been discovered for existing anticancer, antifungal, anthelmintic, and anti-inflammatory drugs. In this review, we discuss the antimicrobial properties of gallium compounds, 5-fluorouracil, ciclopirox, diflunisal, and some other FDA-approved drugs and argue that their repurposing for the treatment of bacterial infections, including those that are multidrug resistant, is a feasible strategy. © 2015 Rangel-Vega, Bernstein, Mandujano-Tinoco, García-Contreras and García-Contreras.

Contreras A.V.,National Autonomous University of Mexico | Contreras A.V.,National Institute of Genomic Medicine | Torres N.,National Institute of Medical science and Nutrition Salvador Zubiran | Tovar A.R.,National Institute of Medical science and Nutrition Salvador Zubiran
Advances in Nutrition | Year: 2013

Peroxisome proliferator-activated receptors (PPARs) are transcription factors that belong to the superfamily of nuclear hormone receptors and regulate the expression of several genes involved in metabolic processes that are potentially linked to the development of some diseases such as hyperlipidemia, diabetes, and obesity. One type of PPAR, PPAR-α, is a transcription factor that regulates the metabolism of lipids, carbohydrates, and amino acids and is activated by ligands such as polyunsaturated fatty acids and drugs used to treat dyslipidemias. There is evidence that genetic variants within the PPARα gene have been associated with a risk of the development of dyslipidemia and cardiovascular disease by influencing fasting and postprandial lipid concentrations; the gene variants have also been associated with an acceleration of the progression of type 2 diabetes. The interactions between genetic PPARα variants and the response to dietary factors will help to identify individuals or populations who can benefit from specific dietary recommendations. Interestingly, certain nutritional conditions, such as the prolonged consumption of a protein-restricted diet, can produce long-lasting effects on PPARα gene expression through modifications in the methylation of a specific locus surrounding the PPARα gene. Thus, this review underlines our current knowledge about the important role of PPAR-α as a mediator of the metabolic response to nutritional and environmental factors. © 2013 American Society for Nutrition.

Romero-Cordoba S.L.,National Institute of Genomic Medicine | Salido-Guadarrama I.,National Institute of Genomic Medicine | Rodriguez-Dorantes M.,National Institute of Genomic Medicine | Hidalgo-Miranda A.,National Institute of Genomic Medicine
Cancer Biology and Therapy | Year: 2014

microRNAs (miRNAs) are non coding RNAs with different biological functions and pathological implications. Given their role as post-transcriptional gene expression regulators, they are involved in several important physiological processes like development, cell differentiation and cell signaling. miRNAs act as modulators of gene expression programs in different diseases, particularly in cancer, where they act through the repression of genes which are critical for carcinogenesis. The expression level of mature miRNAs is the result of a fine mechanism of biogenesis, carried out by different enzymatic complexes that exert their function at transcriptional and post-transcriptional levels. In this review, we will focus our discussion on the alterations in the miRNA biogenesis machinery, and its impact on the establishment and development of cancer programs. © Sandra L Romero-Cordoba, Ivan Salido-Guadarrama, Mauricio Rodriguez-Dorantes, and Alfredo Hidalgo-Miranda.

Rodriguez E.E.,CINVESTAV | Rodriguez E.E.,Autonomous University of Hidalgo | Hernandez-Lemus E.,National Institute of Genomic Medicine | Hernandez-Lemus E.,National Autonomous University of Mexico | And 3 more authors.
PLoS ONE | Year: 2011

The analysis of the interaction and synchronization of relatively large ensembles of neurons is fundamental for the understanding of complex functions of the nervous system. It is known that the temporal synchronization of neural ensembles is involved in the generation of specific motor, sensory or cognitive processes. Also, the intersegmental coherence of spinal spontaneous activity may indicate the existence of synaptic neural pathways between different pairs of lumbar segments. In this study we present a multichannel version of the detrended fluctuation analysis method (mDFA) to analyze the correlation dynamics of spontaneous spinal activity (SSA) from time series analysis. This method together with the classical detrended fluctuation analysis (DFA) were used to find out whether the SSA recorded in one or several segments in the spinal cord of the anesthetized cat occurs either in a random or in an organized manner. Our results are consistent with a non-random organization of the sets of neurons involved in the generation of spontaneous cord dorsum potentials (CDPs) recorded either from one lumbar segment (DFA-α mean = 1.04±0.09) or simultaneously from several lumbar segments (mDFA-α mean = 1.01±0.06), where α>0.5 indicates randomness while α>0.5 indicates long-term correlations. To test the sensitivity of the mDFA method we also examined the effects of small spinal lesions aimed to partially interrupt connectivity between neighboring lumbosacral segments. We found that the synchronization and correlation between the CDPs recorded from the L5 and L6 segments in both sides of the spinal cord were reduced when a lesion comprising the left dorsal quadrant was performed between the segments L5 and L6 (mDFA-α = 0.992 as compared to initial conditions mDFA-α = 1.186). The synchronization and correlation were reduced even further after a similar additional right spinal lesion (mDFA-α = 0.924). In contrast to the classical methods, such as correlation and coherence quantification that define a relation between two sets of data, the mDFA method properly reveals the synchronization of multiple groups of neurons in several segments of the spinal cord. This method is envisaged as a useful tool to characterize the structure of higher order ensembles of cord dorsum spontaneous potentials after spinal cord or peripheral nerve lesions. © 2011 Rodríguez et al.

Hernandez-Lemus E.,National Institute of Genomic Medicine | Hernandez-Lemus E.,National Autonomous University of Mexico | Correa-Rodriguez M.D.,National Institute of Genomic Medicine | Correa-Rodriguez M.D.,National Autonomous University of Mexico
PLoS ONE | Year: 2011

In this work we studied memory and irreversible transport phenomena in a non-equilibrium thermodynamical model for genomic transcriptional regulation. Transcriptional regulation possess an extremely complex phenomenology, and it is, of course, of foremost importance in organismal cell development and in the pathogenesis of complex diseases. A better understanding of the way in which these processes occur is mandatory to optimize the construction of gene regulatory networks, but also to connect these networks with multi-scale phenomena (e.g. metabolism, signalling pathways, etc.) under an integrative Systems Biology-like vision. In this paper we analyzed three simple mechanisms of genetic stimulation: an instant pulse, a periodic biochemical signal and a saturation process with sigmoidal kinetics and from these we derived the system's thermodynamical response, in the form of, for example, anomalous transcriptional bursts. © 2011 Hernández-Lemus, Correa-Rodríguez.

Vazquez-Santillan K.,National Institute of Genomic Medicine | Melendez-Zajgla J.,National Institute of Genomic Medicine | Jimenez-Hernandez L.,National Institute of Genomic Medicine | Martinez-Ruiz G.,National Institute of Genomic Medicine | Maldonado V.,National Institute of Genomic Medicine
Cellular Oncology | Year: 2015

Background: Cancer stem cells (CSCs) are regulated by several signaling pathways that ultimately control their maintenance and expansion. NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) forms a protein complex that controls DNA transcription and, as such, plays an important role in proliferation, inflammation, angiogenesis, invasion and metastasis. The NF-κB signaling pathway, which has been found to be constitutively activated in CSCs from a variety of cancers, participates in the maintenance, expansion, proliferation and survival of CSCs. Targeted disruption of this pathway may profoundly impair the adverse phenotype of CSCs and may provide a therapeutic opportunity to remove the CSC fraction. In particular, it may be attractive to use specific NF-κB inhibitors in chronic therapeutic schemes to reduce disease progression. Exceptional low toxicity profiles of these inhibitors are a prerequisite for use in combined treatment regimens and to avoid resistance. Conclusion: Although still preliminary, recent evidence shows that such targeted strategies may be useful in adjuvant chemo-preventive settings. © 2015, International Society for Cellular Oncology.

Hernandez-Lemus E.,National Institute of Genomic Medicine | Hernandez-Lemus E.,National Autonomous University of Mexico
Frontiers in Physiology | Year: 2013

Systems biology analyses in cancer are rapidly changing from merely descriptive efforts in the high-throughput experimental works and overtly technical, calculation-centered studies in computational systems biology; toward a more functional, mechanistic paradigm. The ultimate goal of cancer systems biology nowadays is thus, unraveling the mechanisms of action, regulation and control in the complex tangle of biochemical and biophysical interactions behind cancer biology. An outstanding example of this trend is given in the paper by Kessler and coworkers (2013). On this work, the authors combine ideas from gene expression profiling for phenotypic classification (Hedenfalk, 2002; Subramanian et al., 2005), of signaling pathways (Haynes et al., 2013; Leiserson et al., 2013) and of network modularity (Hintze and Adami, 2008; Jiang et al., 2008), in order to show how molecular physiology (i.e., understanding the physiological mechanisms of disease from a molecular standpoint) may have many clues leading to better prognosis and treatment of cancer. © 2013 Hernandez-Lemus.

Hernandez-Lemus E.,National Institute of Genomic Medicine
Journal of Thermodynamics | Year: 2012

Signal transduction inside and across the cells, also called cellular signaling, is key to most biological functions and is ultimately related with both life and death of the organisms. The processes giving rise to the propagation of biosignals are complex and extremely cooperative and occur in a far-from thermodynamic equilibrium regime. They are also driven by activation kinetics strongly dependent on local energetics. For these reasons, a nonequilibrium thermodynamical description, taking into account not just the activation of second messengers, but also transport processes and dissipation is desirable. Here we present a proposal for such a formalism, that considers cells as small thermodynamical systems and incorporates the role of fluctuations as intrinsic to the dynamics in a spirit guided by mesoscopic nonequilibrium thermodynamics. We present also a minimal model for cellular signaling that includes contributions from activation, transport, and intrinsic fluctuations. We finally illustrate its feasibility by considering the case of FAS signaling which is a vital signal transduction pathway that determines either cell survival or death by apoptosis. © 2012 Enrique Hernández-Lemus.

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