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News Article | May 4, 2017
Site: www.eurekalert.org

LA JOLLA--(May 4, 2017) Salk Institute scientists have developed a novel technology to correct disease-causing aberrations in the chemical tags on DNA that affect how genes are expressed. These types of chemical modifications, collectively referred to as epigenetics or the epigenome, are increasingly being considered as important as the genomic sequence itself in development and disease. The new Salk technology, which is described in the journal Science on May 4, 2017, was used to model mutations in the epigenome associated with colon cancer and to restore proper methylation patterns in stem cells derived from patients suffering from Angelman syndrome (AS), a rare neurodegenerative disorder often misdiagnosed as autism. In addition to modeling and treating epigenetic disorders, the technology also holds promise for studying human development and biology in general. "We are excited at how many new avenues this work opens up for understanding disease processes and developing effective new therapies," says Salk Professor Juan Carlos Izpisua Belmonte, senior author of the paper and holder of Salk's Roger Guillemin Chair. "It was a giant step to discover how to edit the genome--this technology to edit the epigenome is another leap forward." Izpisua Belmonte's lab recently pioneered a method to modify genes in nondividing cells, which make up the majority of adult tissues. The new technique goes beyond genes to target the most common type of epigenetic change, called DNA methylation, in which chemical tags called methyl groups attach to DNA. Typically these tags mark the gene as ready to be turned on or off. More and more, scientists are learning that DNA methylation is involved in a range of physiological and pathological processes from embryonic development to the onset of certain diseases later in life, including cancer. Researchers have discovered ways of altering methylation status on short DNA sequences, but no one has been able to make the changes stick over a broad range (a prerequisite for proper gene activation or inactivation) until now. Because 80 percent of mammalian DNA is methylated, the Izpisua Belmonte lab was curious about regions that are unmethylated. Paradoxically, these regions are often rich in potential methylation sites and tend to be close to regions of genes where transcription of genetic information begins. Yet somehow these regions, which are called CpG islands, normally remain unmethylated. The researchers hypothesized that interfering with CpG islands might trigger new methylation. To test this hypothesis, the team first used molecular tools to insert DNA without CpGs into the island close to the MLH1 gene. MLH1 is normally unmethylated but leads to an increased risk of colon cancer if it becomes methylated. The team was able to mimic the aberrant methylation in the colon cancer gene as a proof of principle to begin to understand how abnormal methylation is associated with cancers. "What is interesting about CpG islands is that they resist methylation," says Yuta Takahashi, a Salk research associate and first author of the paper. "But by introducing CpG-free DNA, we can override the machinery that blocks it and then induce DNA methylation of the entire island." Knowing they could induce methylation where it doesn't belong, the team next tried to attach methyl tags where they do belong on a genome but are missing, such as in some diseases. Angelman syndrome (AS) results from aberrant DNA methylation, which causes a loss of the UBE3A protein in neurons. This leads to cognitive deficits in patients. By using their technology, the team corrected the abnormal DNA methylation and restored UBE3A protein levels in AS neuronal cells in a dish. Most exciting, according to the researchers, was the fact that all the methylation patterns they introduced were stable over time, which has not been true of other epigenetic technologies. Even removing the CpG-free DNA did not affect the new methylation. The finding offers a way to rewrite epigenetic marks on CpG islands, as well as providing insight into the mechanism by which CpG islands are protected from DNA methylation. "It's wonderful that we have developed a new technology that allows for robust editing of the DNA methylome at CpG islands in pluripotent stem cells, which will help develop cell-replacement therapeutics for epigenetic disorders," says Jun Wu, a Salk staff scientist and one of the paper's coauthors. "But by discovering the underlying mechanisms of DNA methylation, we hope to do even more with this technology." Other authors included Keiichiro Suzuki, Paloma Martinez Redondo, Mo Li, Hsin-Kai Liao, Min-Zu Wu, Reyna Hernández-Benítez, Tomoaki Hishida, Maxim Nikolaievich Shokhirev, Concepcion Rodriguez Esteban and Ignacio Sancho-Martinez of the Salk Institute. The work was funded by the NIH-National Cancer Institute (NCI), the Chapman Foundation, and The Leona M. and Harry B. Helmsley Charitable Trust, UCAM and the G. Harold and Leila Y. Mathers Charitable Foundation. About the Salk Institute for Biological Studies: Every cure has a starting point. The Salk Institute embodies Jonas Salk's mission to dare to make dreams into reality. Its internationally renowned and award-winning scientists explore the very foundations of life, seeking new understandings in neuroscience, genetics, immunology, plant biology and more. The Institute is an independent nonprofit organization and architectural landmark: small by choice, intimate by nature and fearless in the face of any challenge. Be it cancer or Alzheimer's, aging or diabetes, Salk is where cures begin. Learn more at: salk.edu.


Munoz Devesa A.,UCAM | Morales Moreno I.,UCAM | Galan Gonzalez Serna J.M.,University of Seville
Index de Enfermeria | Year: 2014

All human beings suffer, especially during the imbalance produced by diseases. This is the reason why knowing what spiritual suffering is and what spiritual health is it is an important objective that must be reached by nursing interventions. Other-wise, person in a whole sense is not being respected, dignity is not recognized, health is dehumanized and there is a lack of quality in the provided nursing care. We also have to bear in mind that this health problem affects other areas of human life, being spirituality one of the factors that can develop a stronger influence in the welfare of the person or in the recovery time.In this article we try to describe human suffering, included in the spiritual area and its nursing care. Without including that, we can’t speak about holism. © 2014, Fundacion Index. All rights reserved.


Vallejo F.,CSIC - Center of Edafology and Applied Biology of the Segura | Larrosa M.,CSIC - Center of Edafology and Applied Biology of the Segura | Escudero E.,University of Murcia | Zafrilla M.P.,UCAM | And 5 more authors.
Journal of Agricultural and Food Chemistry | Year: 2010

Orange juice is a very rich source of dietary flavanones. The effect of flavanone concentration and solubility of orange beverages on their bioavailability has been studied in a crossover study with 10 healthy volunteers. Five different beverages with different flavanone concentrations were evaluated. Commercial orange juices (29.2-70.3 mg of flavanones/100 mL) were compared with experimental orange beverages in which the flavanone concentration was enhanced (110.2 mg/100 mL). Hesperetin and naringenin glucuronides and sulfates were detected and quantified in plasma and urine. The study shows that the solubility of the flavanones, and particularly that of hesperidin, in the juice is a key factor for the bioavailability as flavanone excretion and the Cmax in plasma correlate well with the soluble flavanone concentration in the juice, whereas it has no correlation with the total flavanone intake. In addition, a large interindividual variation was observed, this being consistent for each individual after the intake of the different beverages, suggesting that flavanone bioavailability is also dependent on the occurrence of specific microbiota that is able to remove the rutinosides from the juice glycosides, which results in aglycones that are then absorbed from the gut. © 2010 American Chemical Society.


News Article | December 19, 2016
Site: www.medicalnewstoday.com

Graying hair, crow's feet, an injury that's taking longer to heal than when we were 20 - faced with the unmistakable signs of aging, most of us have had a least one fantasy of turning back time. Now, scientists at the Salk Institute have found that intermittent expression of genes normally associated with an embryonic state can reverse the hallmarks of old age. This approach, which not only prompted human skin cells in a dish to look and behave young again, also resulted in the rejuvenation of mice with a premature aging disease, countering signs of aging and increasing the animals' lifespan by 30 percent. The early-stage work provides insight both into the cellular drivers of aging and possible therapeutic approaches for improving human health and longevity. "Our study shows that aging may not have to proceed in one single direction," says Juan Carlos Izpisua Belmonte, a professor in Salk's Gene Expression Laboratory and senior author of the paper appearing in the Cell. "It has plasticity and, with careful modulation, aging might be reversed." As people in modern societies live longer, their risk of developing age-related diseases goes up. In fact, data shows that the biggest risk factor for heart disease, cancer and neurodegenerative disorders is simply age. One clue to halting or reversing aging lies in the study of cellular reprogramming, a process in which the expression of four genes known as the Yamanaka factors allows scientists to convert any cell into induced pluripotent stem cells (iPSCs). Like embryonic stem calls, iPSCs are capable of dividing indefinitely and becoming any cell type present in our body. "What we and other stem-cell labs have observed is that when you induce cellular reprogramming, cells look younger," says Alejandro Ocampo, a research associate and first author of the paper. "The next question was whether we could induce this rejuvenation process in a live animal." While cellular rejuvenation certainly sounds desirable, a process that works for laboratory cells is not necessarily a good idea for an entire organism. For one thing, although rapid cell division is critical in growing embryos, in adults such growth is one of the hallmarks of cancer. For another, having large numbers of cells revert back to embryonic status in an adult could result in organ failure, ultimately leading to death. For these reasons, the Salk team wondered whether they could avoid cancer and improve aging characteristics by inducing the Yamanaka factors for a short period of time. To find out, the team turned to a rare genetic disease called progeria. Both mice and humans with progeria show many signs of aging including DNA damage, organ dysfunction and dramatically shortened lifespan. Moreover, the chemical marks on DNA responsible for the regulation of genes and protection of our genome, known as epigenetic marks, are prematurely dysregulated in progeria mice and humans. Importantly, epigenetic marks are modified during cellular reprogramming. Using skin cells from mice with progeria, the team induced the Yamanaka factors for a short duration. When they examined the cells using standard laboratory methods, the cells showed reversal of multiple aging hallmarks without losing their skin-cell identity. "In other studies scientists have completely reprogrammed cells all the way back to a stem-cell-like state," says co-first author Pradeep Reddy, also a Salk research associate. "But we show, for the first time, that by expressing these factors for a short duration you can maintain the cell's identity while reversing age-associated hallmarks." Encouraged by this result, the team used the same short reprogramming method during cyclic periods in live mice with progeria. The results were striking: Compared to untreated mice, the reprogrammed mice looked younger; their cardiovascular and other organ function improved and - most surprising of all - they lived 30 percent longer, yet did not develop cancer. On a cellular level, the animals showed the recovery of molecular aging hallmarks that are affected not only in progeria, but also in normal aging. "This work shows that epigenetic changes are at least partially driving aging," says co-first author Paloma Martinez-Redondo, another Salk research associate. "It gives us exciting insights into which pathways could be targeted to delay cellular aging." Lastly, the Salk scientists turned their efforts to normal, aged mice. In these animals, the cyclic induction of the Yamanaka factors led to improvement in the regeneration capacity of pancreas and muscle. In this case, injured pancreas and muscle healed faster in aged mice that were reprogrammed, indicating a clear improvement in the quality of life by cellular reprogramming. "Obviously, mice are not humans and we know it will be much more complex to rejuvenate a person," says Izpisua Belmonte. "But this study shows that aging is a very dynamic and plastic process, and therefore will be more amenable to therapeutic interventions than what we previously thought." The Salk researchers believe that induction of epigenetic changes via chemicals or small molecules may be the most promising approach to achieve rejuvenation in humans. However, they caution that, due to the complexity of aging, these therapies may take up to 10 years to reach clinical trials. Other authors included: Aida Platero-Luengo, Fumiyuki Hatanaka, Tomoaki Hishida, Mo Li, David Lam, Masakazu Kurita, Ergin Beyret, Toshikazu Araoka, Eric Vazquez-Ferrer, David Donoso, Jose Luis Roman, Jinna Xu and Concepcion Rodriguez of the Salk Institute; Estrella Nuñez Delicado of Universidad Católica San Antonio de Murcia; Gabriel Núñez of the University of Michigan Medical School; Josep Maria Campistol of Hosplital Clinic of Barcelona and Isabel Guillén and Pedro Guillén of Fundación Dr. Pedro Guillén. The work and the researchers involved were supported in part by a National Institutes of Health Ruth L. Kirschstein National Research Service Award Individual Postdoctoral Fellowship, the Muscular Dystrophy Association, Fundación Alfonso Martin Escudero, the Hewitt Foundation, the Uehara Memorial Foundation, the Nomis Foundation, a JSPS Postdoctoral Fellowship for Research Abroad, the University of California, San Diego, the G. Harold and Leila Y. Mathers Charitable Foundation, The Leona M. and Harry B. Helmsley Charitable Trust (2012-PG-MED002), The Glenn Foundation, Universidad Católica San Antonio de Murcia (UCAM) and Fundación Dr. Pedro Guillén. Article: In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming, Juan Carlos Izpisua Belmonte, Cell, doi: 10.1016/j.cell.2016.11.052, published 15 December 2016.


News Article | December 15, 2016
Site: www.eurekalert.org

LA JOLLA -- (Dec. 15, 2016) Graying hair, crow's feet, an injury that's taking longer to heal than when we were 20 -- faced with the unmistakable signs of aging, most of us have had a least one fantasy of turning back time. Now, scientists at the Salk Institute have found that intermittent expression of genes normally associated with an embryonic state can reverse the hallmarks of old age. This approach, which not only prompted human skin cells in a dish to look and behave young again, also resulted in the rejuvenation of mice with a premature aging disease, countering signs of aging and increasing the animals' lifespan by 30 percent. The early-stage work provides insight both into the cellular drivers of aging and possible therapeutic approaches for improving human health and longevity. "Our study shows that aging may not have to proceed in one single direction," says Juan Carlos Izpisua Belmonte, a professor in Salk's Gene Expression Laboratory and senior author of the paper appearing in the December 15, 2016 issue of Cell. "It has plasticity and, with careful modulation, aging might be reversed." As people in modern societies live longer, their risk of developing age-related diseases goes up. In fact, data shows that the biggest risk factor for heart disease, cancer and neurodegenerative disorders is simply age. One clue to halting or reversing aging lies in the study of cellular reprogramming, a process in which the expression of four genes known as the Yamanaka factors allows scientists to convert any cell into induced pluripotent stem cells (iPSCs). Like embryonic stem calls, iPSCs are capable of dividing indefinitely and becoming any cell type present in our body. "What we and other stem-cell labs have observed is that when you induce cellular reprogramming, cells look younger," says Alejandro Ocampo, a research associate and first author of the paper. "The next question was whether we could induce this rejuvenation process in a live animal." While cellular rejuvenation certainly sounds desirable, a process that works for laboratory cells is not necessarily a good idea for an entire organism. For one thing, although rapid cell division is critical in growing embryos, in adults such growth is one of the hallmarks of cancer. For another, having large numbers of cells revert back to embryonic status in an adult could result in organ failure, ultimately leading to death. For these reasons, the Salk team wondered whether they could avoid cancer and improve aging characteristics by inducing the Yamanaka factors for a short period of time. To find out, the team turned to a rare genetic disease called progeria. Both mice and humans with progeria show many signs of aging including DNA damage, organ dysfunction and dramatically shortened lifespan. Moreover, the chemical marks on DNA responsible for the regulation of genes and protection of our genome, known as epigenetic marks, are prematurely dysregulated in progeria mice and humans. Importantly, epigenetic marks are modified during cellular reprogramming. Using skin cells from mice with progeria, the team induced the Yamanaka factors for a short duration. When they examined the cells using standard laboratory methods, the cells showed reversal of multiple aging hallmarks without losing their skin-cell identity. "In other studies scientists have completely reprogrammed cells all the way back to a stem-cell-like state," says co-first author Pradeep Reddy, also a Salk research associate. "But we show, for the first time, that by expressing these factors for a short duration you can maintain the cell's identity while reversing age-associated hallmarks." Encouraged by this result, the team used the same short reprogramming method during cyclic periods in live mice with progeria. The results were striking: Compared to untreated mice, the reprogrammed mice looked younger; their cardiovascular and other organ function improved and--most surprising of all--they lived 30 percent longer, yet did not develop cancer. On a cellular level, the animals showed the recovery of molecular aging hallmarks that are affected not only in progeria, but also in normal aging. "This work shows that epigenetic changes are at least partially driving aging," says co-first author Paloma Martinez-Redondo, another Salk research associate. "It gives us exciting insights into which pathways could be targeted to delay cellular aging." Lastly, the Salk scientists turned their efforts to normal, aged mice. In these animals, the cyclic induction of the Yamanaka factors led to improvement in the regeneration capacity of pancreas and muscle. In this case, injured pancreas and muscle healed faster in aged mice that were reprogrammed, indicating a clear improvement in the quality of life by cellular reprogramming. "Obviously, mice are not humans and we know it will be much more complex to rejuvenate a person," says Izpisua Belmonte. "But this study shows that aging is a very dynamic and plastic process, and therefore will be more amenable to therapeutic interventions than what we previously thought." The Salk researchers believe that induction of epigenetic changes via chemicals or small molecules may be the most promising approach to achieve rejuvenation in humans. However, they caution that, due to the complexity of aging, these therapies may take up to 10 years to reach clinical trials. Other authors included: Aida Platero-Luengo, Fumiyuki Hatanaka, Tomoaki Hishida, Mo Li, David Lam, Masakazu Kurita, Ergin Beyret, Toshikazu Araoka, Eric Vazquez-Ferrer, David Donoso, Jose Luis Roman, Jinna Xu and Concepcion Rodriguez of the Salk Institute; Estrella Nuñez Delicado of Universidad Católica San Antonio de Murcia; Gabriel Núñez of the University of Michigan Medical School; Josep Maria Campistol of Hosplital Clinic of Barcelona and Isabel Guillén and Pedro Guillén of Fundación Dr. Pedro Guillén. The work and the researchers involved were supported in part by a National Institutes of Health Ruth L. Kirschstein National Research Service Award Individual Postdoctoral Fellowship, the Muscular Dystrophy Association, Fundación Alfonso Martin Escudero, the Hewitt Foundation, the Uehara Memorial Foundation, the Nomis Foundation, a JSPS Postdoctoral Fellowship for Research Abroad, the University of California, San Diego, the G. Harold and Leila Y. Mathers Charitable Foundation, The Leona M. and Harry B. Helmsley Charitable Trust (2012-PG-MED002), The Glenn Foundation, Universidad Católica San Antonio de Murcia (UCAM) and Fundación Dr. Pedro Guillén. About the Salk Institute for Biological Studies: Every cure has a starting point. The Salk Institute embodies Jonas Salk's mission to dare to make dreams into reality. Its internationally renowned and award-winning scientists explore the very foundations of life, seeking new understandings in neuroscience, genetics, immunology, plant biology and more. The Institute is an independent nonprofit organization and architectural landmark: small by choice, intimate by nature and fearless in the face of any challenge. Be it cancer or Alzheimer's, aging or diabetes, Salk is where cures begin. Learn more at: salk.edu.


News Article | December 15, 2016
Site: www.eurekalert.org

Scientists have rolled back time for live mice through systemic cellular reprogramming, according to a study published December 15 in Cell. In mice carrying a mutation leading to premature aging, reprogramming of chemical marks in the genome, known as epigenetic marks, reduced many signs of aging in the mice and extended their lifespan on average from 18 weeks to 24. The study suggests that epigenetic changes drive the aging process, and that those changes may be malleable. "We did not correct the mutation that causes premature aging in these mice," says lead investigator Juan Carlos Izpisua Belmonte, a professor in the Salk Institute of Biological Science's Gene Expression Laboratory. "We altered aging by changing the epigenome, suggesting that aging is a plastic process." This is the first report in which cellular reprogramming extends lifespan in a live animal. Previous efforts resulted in mice that either died immediately or developed extensive tumors. The Salk team used a partial cellular reprogramming approach that did not cause tumors or death. "We were surprised and excited to see that we were able to prolong the lifespan by in vivo reprogramming," says co-first author Pradeep Reddy. Cellular reprogramming turns an adult cell, such as a skin cell, into an induced pluripotent stem (iPS) cell. IPS cells have high proliferation rates and are not yet specialized to perform functions, such as being part of the skin. Reprogramming involves inducing the expression of four factors, called Yamanaka factors, in cells. The factors must be expressed for 2 to 3 weeks for cells to reach pluripotency. The Salk team used partial reprogramming, which induced expression of Yamanaka factors for just 2 to 4 days. Cells do not reach pluripotency. Rather, a cell that starts off as a skin cell remains a skin cell. But signs of age-associated dysfunction in the cell diminish. In this study, partial reprogramming of cells in vitro reduced DNA damage accumulation and restored nuclear structure. "These changes are the result of epigenetic remodeling in the cell," says Izpisua Belmonte. Epigenetic marks, which change over a lifetime in response to environmental changes, regulate and protect the genome. Some marks turn on specialized functions, such as skin cell machinery in a skin cell, and turn off mechanisms that aren't needed, such as liver cell machinery. "During aging, marks are added, removed, and modified," says co-first author Alejandro Ocampo. "It's clear that the epigenome is changing as we get older." The team induced expression of Yamanaka factors in all cells of the organism using their partial reprogramming approach. Several organs improved. For instance, tissue from skin, spleen, kidney and stomach all had improved appearance when inspected under a microscope. The cardiovascular system, which often fails and causes early death in these prematurely aging mice, also showed improvements in structure and function. "It is difficult to say specifically why the animal lives longer," says co-first author Paloma Martinez-Redondo. "But we know that the expression of these factors is inducing changes in the epigenome, and those are leading to benefits at the cellular and organismal level." The team also tested applications of partial reprogramming in models of injury in mice. In this study, partial reprogramming enhanced the regeneration of muscle tissue and beta cells in the pancreas following injury. Next steps will involve learning more about how the epigenome changes during partial reprogramming. "We need to go back and explore which marks are changing and driving the aging process," says Izpisua Belmonte. This study was supported by the G. Harold and Leila Y. Mathers Charitable Foundation, The Leona M. and Harry B. Helmsley Charitable Trust, The Glenn Foundation, Universidad Católica San Antonio de Murcia (UCAM), and Fundación Dr. Pedro Guillen. Cell, Ocampo et al.: "In vivo amelioration of age-associated hallmarks by partial reprogramming." http://www.cell.com/cell/fulltext/S0092-8674(16)31664-6 Cell (@CellCellPress), the flagship journal of Cell Press, is a bimonthly journal that publishes findings of unusual significance in any area of experimental biology, including but not limited to cell biology, molecular biology, neuroscience, immunology, virology and microbiology, cancer, human genetics, systems biology, signaling, and disease mechanisms and therapeutics. Visit: http://www. . To receive Cell Press media alerts, contact press@cell.com.


This work focuses its interest in the difficult relationships between health and social disciplines when facing a complex problem as alcohol consumption. The question is whether the scientific practice has the capacity to reduce risks, or on the contrary it is necessary to protect ourselves from the dangers which it produces. Social scientists complain about the limited use that medicine makes of the vast existing heritage about the cultural-based alcoholism. At the same time scientists criticize the inefficiency of biomedical approaches. In this article, we highlight the importance of a contextualized analysis about the alcohol consumption that takes into account the functions and consequences from the social structure that gives it collective and subjective significance. Current paradoxes in the social government of dependencies are manifested. Looking to the phenomenon of collective consumption of alcohol among young people, we suggest alternative approaches that incorporate the mean-ings and intervention capacity of the subjects themselves. © 2014, Fundacion Index. All rights reserved.


Hastie P.A.,Auburn University | de Ojeda D.M.,Colegio de Educacion Infantil | Luquinc A.C.,UCAM
Physical Education and Sport Pedagogy | Year: 2011

Background: In 2005, Wallhead and O'Sullivan presented a review of research on the Sport Education model. In that review, the authors identified certain strengths of the model (particularly persistent team membership) in facilitating student engagement within student-centered learning tasks. Other areas (such as student leadership skills) were considered as potentially problematic. Suggestions were also made for future research. Purpose: The three purposes of this review were to conduct a review of research on Sport Education since the 2005 analysis, to identify any new trends in research since the original review, and to describe the extent to which the limitations and future research directions of Wallhead and O'Sullivan have been addressed. Data collection: Papers for analysis were selected through searches of EBSCO databases with the main identifier 'sport education'. Further journal articles were then obtained through the citations and references in the original documents. Data analysis: Papers were initially categorized according to the following dimensions: country of origin, focus, participants, sport and length of season, data courses, analysis and results. They were then discussed in terms of the five common content standards and aims of physical education (e.g. skill and fitness development, personal and social responsibility) used in the 2005 review. Findings: Thirty-eight papers were identified that satisfied the selection criteria, with all content standards receiving attention. Since the 2005 review, there been not only an expansion in the number of studies relating to Sport Education, but also the initiation of research in a number of new contexts, as well as those focused on new research questions. An analytic induction of these papers has placed them into three categories: (1) expanded sites of implementation; (2) students' motivational responses; and (3) learning to teach Sport Education. Conclusions: Studies of Sport Education now take place in more diverse settings than before, and continue to progress with more sophisticated research designs and larger sample sizes. Still, more investigation is needed in the areas of peer instruction and the transfer of school-based learning to community sport. © 2011 Association for Physical Education.


A phylogeny is a tree that relates taxonomic units based on their similarity over a set of characteristics. The phylogeny problem under the parsimony criterion consists in finding a phylogeny with a minimum number of evolutionary steps. We propose hybrid heuristic methods - based on GRASP, path-relinking and genetic algorithm methodologies - to build a phylogeny while minimizing parsimony. Computational experiments using benchmark conditions are reported, and the results obtained by the proposed hybrid heuristics are compared with the solutions obtained by a traditional GRASP (without hybridization) heuristic and with previously reported solutions in the literature. The experimental results illustrate that the proposed heuristics are efficient in terms of solution quality and time-to-target-value.


Dietrich G.,University of Paris Descartes | Bredin J.,UCAM | Kerlirzin Y.,University of Paris Descartes
Motor Control | Year: 2010

The aim of this article is to elaborate a general framework for modeling dual opposition activities, or more generally, dual interaction. The main hypothesis is that opposition behavior can be measured directly from a global variable and that the relative distance between the two subjects can be this parameter. Moreover, this parameter should be considered as multidimensional parameter depending not only on the dynamics of the subjects but also on the "internal" parameters of the subjects, such as sociological and/or emotional states. Standard and simple mechanical formalization will be used to model this multifactorial distance. To illustrate such a general modeling methodology, this model was compared with actual data from an opposition activity like Japanese fencing (kendo). This model captures not only coupled coordination, but more generally interaction in two-subject activities. © 2010 Human Kinetics, Inc.

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