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Author (up) Amaku, M.; Coutinho, F.A.B.; Massad, E. file  url
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  Title Why dengue and yellow fever coexist in some areas of the world and not in others? Type Journal Article
  Year 2011 Publication Bio Systems Abbreviated Journal Biosystems  
  Volume 106 Issue 2-3 Pages 111-120  
  Keywords Adaptive Immunity/*immunology; Aedes/*virology; Africa/epidemiology; Animals; Asia/epidemiology; Computer Simulation; *Demography; Dengue/*epidemiology/immunology/transmission; Humans; Insect Vectors/*virology; *Models, Biological; South America/epidemiology; Species Specificity; Yellow Fever/*epidemiology/immunology/transmission  
  Abstract Urban yellow fever and dengue coexist in Africa but not in Asia and South America. In this paper, we examine four hypotheses (and various combinations thereof) to explain the absence of yellow fever in urban areas of Asia and South America. In addition, we examine an additional hypothesis that offers an explanation of the coexistence of the infections in Africa while at the same time explaining their lack of coexistence in Asia. The hypotheses we tested to explain the nonexistence of yellow fever in Asia are the following: (1) the Asian Aedes aegypti is relatively incompetent to transmit yellow fever; (2) there would exist a competition between dengue and yellow fever viruses within the mosquitoes, as suggested by in vitro studies in which the dengue virus always wins; (3) when an A. aegypti mosquito that is infected by or latent for yellow fever acquires dengue, it becomes latent for dengue due to internal competition within the mosquito between the two viruses; (4) there is an important cross-immunity between yellow fever and other flaviviruses, dengue in particular, such that a person recovered from a bout of dengue exhibits a diminished susceptibility to yellow fever. This latter hypothesis is referred to below as the “Asian hypothesis.” Finally, we hypothesize that: (5) the coexistence of the infections in Africa is due to the low prevalence of the mosquito Aedes albopictus in Africa, as it competes with A. aegypti. We will refer to this latter hypothesis as the “African hypothesis.” We construct a model of transmission that allows all of the above hypotheses to be tested. We conclude that the Asian and the African hypotheses can explain the observed phenomena, whereas other hypotheses fail to do so.  
  Call Number Serial 1532  
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Author (up) Changeux, J.-P. file  url
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  Title The concept of allosteric interaction and its consequences for the chemistry of the brain Type Journal Article
  Year 2013 Publication The Journal of Biological Chemistry Abbreviated Journal J Biol Chem  
  Volume 288 Issue 38 Pages 26969-26986  
  Keywords Allosteric Regulation/physiology; Brain Chemistry/*physiology; History, 20th Century; History, 21st Century; Humans; *Models, Biological; *Molecular Dynamics Simulation; Nerve Tissue Proteins/*metabolism; Portraits as Topic; Prokaryotic Cells/physiology; Allosteric Regulation; Membrane Proteins; Neurons; Nicotinic Acetylcholine Receptors; Synaptic Plasticity  
  Abstract Throughout this Reflections article, I have tried to follow up on the genesis in the 1960s and subsequent evolution of the concept of allosteric interaction and to examine its consequences within the past decades, essentially in the field of the neuroscience. The main conclusion is that allosteric mechanisms built on similar structural principles operate in bacterial regulatory enzymes, gene repressors (and the related nuclear receptors), rhodopsin, G-protein-coupled receptors, neurotransmitter receptors, ion channels, and so on from prokaryotes up to the human brain yet with important features of their own. Thus, future research on these basic cybernetic sensors is expected to develop in two major directions: at the elementary level, toward the atomic structure and molecular dynamics of the conformational changes involved in signal recognition and transduction, but also at a higher level of organization, the contribution of allosteric mechanisms to the modulation of brain functions.  
  Call Number Serial 1878  
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Author (up) Changeux, J.-P. file  url
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  Title The concept of allosteric interaction and its consequences for the chemistry of the brain Type Journal Article
  Year 2013 Publication The Journal of Biological Chemistry Abbreviated Journal J Biol Chem  
  Volume 288 Issue 38 Pages 26969-26986  
  Keywords Allosteric Regulation/physiology; Brain Chemistry/*physiology; History, 20th Century; History, 21st Century; Humans; *Models, Biological; *Molecular Dynamics Simulation; Nerve Tissue Proteins/*metabolism; Portraits as Topic; Prokaryotic Cells/physiology; Allosteric Regulation; Membrane Proteins; Neurons; Nicotinic Acetylcholine Receptors; Synaptic Plasticity  
  Abstract Throughout this Reflections article, I have tried to follow up on the genesis in the 1960s and subsequent evolution of the concept of allosteric interaction and to examine its consequences within the past decades, essentially in the field of the neuroscience. The main conclusion is that allosteric mechanisms built on similar structural principles operate in bacterial regulatory enzymes, gene repressors (and the related nuclear receptors), rhodopsin, G-protein-coupled receptors, neurotransmitter receptors, ion channels, and so on from prokaryotes up to the human brain yet with important features of their own. Thus, future research on these basic cybernetic sensors is expected to develop in two major directions: at the elementary level, toward the atomic structure and molecular dynamics of the conformational changes involved in signal recognition and transduction, but also at a higher level of organization, the contribution of allosteric mechanisms to the modulation of brain functions.  
  Call Number Serial 1888  
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Author (up) Griffin, A.S.; West, S.A.; Buckling, A. file  url
openurl 
  Title Cooperation and competition in pathogenic bacteria Type Journal Article
  Year 2004 Publication Nature Abbreviated Journal Nature  
  Volume 430 Issue 7003 Pages 1024-1027  
  Keywords Altruism; Analysis of Variance; *Biological Evolution; Competitive Behavior; Cooperative Behavior; Host-Parasite Interactions; Humans; *Models, Biological; Pseudomonas aeruginosa/classification/genetics/*pathogenicity/*physiology; Siderophores/*biosynthesis; Virulence  
  Abstract Explaining altruistic cooperation is one of the greatest challenges for evolutionary biology. One solution to this problem is if costly cooperative behaviours are directed towards relatives. This idea of kin selection has been hugely influential and applied widely from microorganisms to vertebrates. However, a problem arises if there is local competition for resources, because this leads to competition between relatives, reducing selection for cooperation. Here we use an experimental evolution approach to test the effect of the scale of competition, and how it interacts with relatedness. The cooperative trait that we examine is the production of siderophores, iron-scavenging agents, in the pathogenic bacterium Pseudomonas aeruginosa. As expected, our results show that higher levels of cooperative siderophore production evolve in the higher relatedness treatments. However, our results also show that more local competition selects for lower levels of siderophore production and that there is a significant interaction between relatedness and the scale of competition, with relatedness having less effect when the scale of competition is more local. More generally, the scale of competition is likely to be of particular importance for the evolution of cooperation in microorganisms, and also the virulence of pathogenic microorganisms, because cooperative traits such as siderophore production have an important role in determining virulence.  
  Call Number Serial 1552  
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Author (up) Phillips, J.C.; Braun, R.; Wang, W.; Gumbart, J.; Tajkhorshid, E.; Villa, E.; Chipot, C.; Skeel, R.D.; Kale, L.; Schulten, K. file  url
doi  openurl
  Title Scalable molecular dynamics with NAMD Type Journal Article
  Year 2005 Publication Journal of Computational Chemistry Abbreviated Journal J Comput Chem  
  Volume 26 Issue 16 Pages 1781-1802  
  Keywords Algorithms; Aquaporins/chemistry; Cell Membrane/chemistry; *Computer Simulation; Glycophorin/chemistry; *Models, Biological; *Models, Chemical; Models, Molecular; Repressor Proteins/chemistry; *Software; Software Design; Static Electricity; Ubiquitin/chemistry  
  Abstract NAMD is a parallel molecular dynamics code designed for high-performance simulation of large biomolecular systems. NAMD scales to hundreds of processors on high-end parallel platforms, as well as tens of processors on low-cost commodity clusters, and also runs on individual desktop and laptop computers. NAMD works with AMBER and CHARMM potential functions, parameters, and file formats. This article, directed to novices as well as experts, first introduces concepts and methods used in the NAMD program, describing the classical molecular dynamics force field, equations of motion, and integration methods along with the efficient electrostatics evaluation algorithms employed and temperature and pressure controls used. Features for steering the simulation across barriers and for calculating both alchemical and conformational free energy differences are presented. The motivations for and a roadmap to the internal design of NAMD, implemented in C++ and based on Charm++ parallel objects, are outlined. The factors affecting the serial and parallel performance of a simulation are discussed. Finally, typical NAMD use is illustrated with representative applications to a small, a medium, and a large biomolecular system, highlighting particular features of NAMD, for example, the Tcl scripting language. The article also provides a list of the key features of NAMD and discusses the benefits of combining NAMD with the molecular graphics/sequence analysis software VMD and the grid computing/collaboratory software BioCoRE. NAMD is distributed free of charge with source code at www.ks.uiuc.edu.  
  Call Number Serial 418  
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Author (up) Speakman, J.R. file  url
doi  openurl
  Title Body size, energy metabolism and lifespan Type Journal Article
  Year 2005 Publication The Journal of Experimental Biology Abbreviated Journal J Exp Biol  
  Volume 208 Issue Pt 9 Pages 1717-1730  
  Keywords Animals; Basal Metabolism/*physiology; *Body Size; Energy Metabolism/*physiology; Free Radicals/metabolism; *Longevity; Mitochondria/metabolism; *Models, Biological; Species Specificity; Temperature  
  Abstract Bigger animals live longer. The scaling exponent for the relationship between lifespan and body mass is between 0.15 and 0.3. Bigger animals also expend more energy, and the scaling exponent for the relationship of resting metabolic rate (RMR) to body mass lies somewhere between 0.66 and 0.8. Mass-specific RMR therefore scales with a corresponding exponent between -0.2 and -0.33. Because the exponents for mass-specific RMR are close to the exponents for lifespan, but have opposite signs, their product (the mass-specific expenditure of energy per lifespan) is independent of body mass (exponent between -0.08 and 0.08). This means that across species a gram of tissue on average expends about the same amount of energy before it dies regardless of whether that tissue is located in a shrew, a cow, an elephant or a whale. This fact led to the notion that ageing and lifespan are processes regulated by energy metabolism rates and that elevating metabolism will be associated with premature mortality--the rate of living theory. The free-radical theory of ageing provides a potential mechanism that links metabolism to ageing phenomena, since oxygen free radicals are formed as a by-product of oxidative phosphorylation. Despite this potential synergy in these theoretical approaches, the free-radical theory has grown in stature while the rate of living theory has fallen into disrepute. This is primarily because comparisons made across classes (for example, between birds and mammals) do not conform to the expectations, and even within classes there is substantial interspecific variability in the mass-specific expenditure of energy per lifespan. Using interspecific data to test the rate of living hypothesis is, however, confused by several major problems. For example, appeals that the resultant lifetime expenditure of energy per gram of tissue is 'too variable' depend on the biological significance rather than the statistical significance of the variation observed. Moreover, maximum lifespan is not a good marker of ageing and RMR is not a good measure of total energy metabolism. Analysis of residual lifespan against residual RMR reveals no significant relationship. However, this is still based on RMR. A novel comparison using daily energy expenditure (DEE), rather than BMR, suggests that lifetime expenditure of energy per gram of tissue is NOT independent of body mass, and that tissue in smaller animals expends more energy before expiring than tissue in larger animals. Some of the residual variation in this relationship in mammals is explained by ambient temperature. In addition there is a significant negative relationship between residual lifespan and residual daily energy expenditure in mammals. A potentially much better model to explore the links of body size, metabolism and ageing is to examine the intraspecific links. These studies have generated some data that support the original rate of living theory and other data that conflict. In particular several studies have shown that manipulating animals to expend more or less energy generate the expected effects on lifespan (particularly when the subjects are ectotherms). However, smaller individuals with higher rates of metabolism live longer than their slower, larger conspecifics. An addition to these confused observations has been the recent suggestion that under some circumstances we might expect mitochondria to produce fewer free radicals when metabolism is higher--particularly when they are uncoupled. These new ideas concerning the manner in which mitochondria generate free radicals as a function of metabolism shed some light on the complexity of observations linking body size, metabolism and lifespan.  
  Call Number Serial 122  
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