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Author (up) Alcock, J.; Maley, C.C.; Aktipis, C.A. file  url
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  Title Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms Type Journal Article
  Year 2014 Publication BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology Abbreviated Journal Bioessays  
  Volume 36 Issue 10 Pages 940-949  
  Keywords Animals; *Biological Evolution; *Feeding Behavior; Gastrointestinal Tract/*microbiology; Humans; *Microbiota; Models, Biological; Obesity/etiology; Cravings; Evolutionary conflict; Host manipulation; Microbiome; Obesity  
  Abstract Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness. We review several potential mechanisms for microbial control over eating behavior including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the vagus nerve, the neural axis between the gut and the brain. We also review the evidence for alternative explanations for cravings and unhealthy eating behavior. Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating.  
  Call Number Serial 2002  
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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) Anderson, J.L.; Albergotti, L.; Proulx, S.; Peden, C.; Huey, R.B.; Phillips, P.C. file  url
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  Title Thermal preference of Caenorhabditis elegans: a null model and empirical tests Type Journal Article
  Year 2007 Publication The Journal of Experimental Biology Abbreviated Journal J Exp Biol  
  Volume 210 Issue Pt 17 Pages 3107-3116  
  Keywords Acclimatization; Animals; Behavior, Animal; Body Temperature Regulation; Caenorhabditis elegans--physiology; Escherichia coli--growth & development; Models, Biological; Temperature  
  Abstract The preferred body temperature of ectotherms is typically inferred from the observed distribution of body temperatures in a laboratory thermal gradient. For very small organisms, however, that observed distribution might misrepresent true thermal preferences. Tiny ectotherms have limited thermal inertia, and so their body temperature and speed of movement will vary with their position along the gradient. In order to separate the direct effects of body temperature on movement from actual preference behaviour on a thermal gradient, we generate a null model (i.e. of non-thermoregulating individuals) of the spatial distribution of ectotherms on a thermal gradient and test the model using parameter values estimated from the movement of nematodes (Caenorhabditis elegans) at fixed temperatures and on a thermal gradient. We show that the standard lab strain N2, which is widely used in thermal gradient studies, avoids high temperature but otherwise does not exhibit a clear thermal preference, whereas the Hawaiian natural isolate CB4856 shows a clear preference for cool temperatures ( approximately 17 degrees C). These differences are not influenced substantially by changes in the starting position of worms in the gradient, the natal temperature of individuals or the presence and physiological state of bacterial food. These results demonstrate the value of an explicit null model of thermal effects and highlight problems in the standard model of C. elegans thermotaxis, showing the value of using natural isolates for tests of complex natural behaviours.  
  Call Number Serial 260  
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Author (up) Arimoto-Kobayashi, S.; Sakata, H.; Mitsu, K.; Tanoue, H. file  url
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  Title A possible photosensitizer: Tobacco-specific nitrosamine, 4-(N-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), induced mutations, DNA strand breaks and oxidative and methylative damage with UVA Type Journal Article
  Year 2007 Publication Mutation Research Abbreviated Journal Mutat Res  
  Volume 632 Issue 1-2 Pages 111-120  
  Keywords Base Sequence; DNA Breaks; DNA Methylation--drug effects, radiation effects; Dose-Response Relationship, Drug; Models, Biological; Molecular Sequence Data; Mutation; Nitrosamines--toxicity; Oxidative Stress--drug effects, radiation effects; Photosensitizing Agents--toxicity; Salmonella typhimurium; Tobacco--chemistry; Ultraviolet Rays--adverse effects  
  Abstract We discovered the directly acting mutagenicity of the tobacco-specific nitrosamine, 4-(N-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), with UVA light (320-400nm) in Ames bacteria and phage M13mp2 in the absence of metabolic activation. We have investigated the spectrum of mutations caused by UVA-activated NNK. The majority (57%) of induced sequence changes were comprised of GC to CG, GC to TA and GC to AT. This suggested that modification of guanine residues was responsible for these mutations. Hence, we explored the formation of 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxodG) and O(6)-methylguanine (O(6)meG) in the DNA. When calf thymus DNA was treated with NNK and UVA, the amount of 8-oxodG/dG and O(6)meG/G in the DNA increased up to 20-fold and 100-fold, respectively, compared with the untreated control. DNA strand breaks were observed following NNK and UVA treatment, and the strand breaks were suppressed in the presence of scavengers for oxygen and NO radical. The formation of NO was also observed in NNK solutions irradiated with UVA. We analyzed the photodynamic spectrum of mutation induction, 8-oxodG formation and NO formation using monochromatic radiation. The patterns of the action spectra were comparable to the absorption spectrum of NNK. We conclude that NNK may act as a photosensitizer in response to UVA to produce NO and other oxidative and alkylative intermediates following the formation of 8-oxodG and O(6)meG in DNA, which may lead to mutations and DNA strand breaks.  
  Call Number Serial 86  
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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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