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    <title>Nature Precedings - Milind Watve</title>
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    <description>Documents posted by Milind Watve</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
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      <title>Evolution of Co-operation When the Strategies are Hidden: The Human Mating Game</title>
      <link>http://dx.doi.org/10.1038/npre.2007.740.1</link>
      <description>Defection is frequently seen in co-operative systems [1-3]. Game theoretical solutions to stabilize cooperation rely on reciprocity and reputation in iterated games[4-5]. One of the basic requirements for reciprocity or reputation building is that the strategies of players and the resulting payoffs should be open at the end of every interaction. For games in which the strategies and payoffs remain hidden, these stabilizing factors are unlikely to work. We examine the evolution of cooperation for hidden-strategy games using human mating game as an example.  Here faithful parenting can be considered as cooperation and extra-pair mating (EPM) or cuckoldry as defection. Cuckoldry may get exposed only occasionally and the genetic benefits of cuckoldry also remain hidden from the players. Along with mate guarding, social policing is enabled in humans by language and gossiping. However, social policing can be invaded by second order free riders. We suggest that opportunistic blackmailing, which is unique to hidden strategy games can act as a keystone strategy in stabilizing co-operation. This can counteract free riding and stabilize policing. A game theoretical model results into a rock &amp;#8211; paper &#8211; scissor (R-P-S) like situation with no evolutionary stable strategy (ESS). Simulations result into a stable or stably oscillating polymorphism. Obligate monogamy is an essential trait in the co-existence. In a gender difference model too, polymorphism is seen in both genders but with different traits predominating in the two genders. The model explains intra-gender, inter-gender as well as cross cultural variability in mating strategies in humans.</description>
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      <pubDate>Tue, 21 Aug 2007 05:37:18 UTC</pubDate>
      <dc:title>Evolution of Co-operation When the Strategies are Hidden: The Human Mating Game</dc:title>
      <dc:identifier>doi:10.1038/npre.2007.740.1</dc:identifier>
      <dc:date>2009-03-04</dc:date>
      <dc:creator>Milind Watve</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-08-21T05:37:18Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Evolutionary Biology</prism:section>
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      <title>Obesity as a perceived social signal</title>
      <link>http://dx.doi.org/10.1038/npre.2008.2711.1</link>
      <description>Fat accumulation has been classically considered as a means of energy storage. Obese people are theorized as metabolically &#8216;thrifty&#8217;, saving energy during times of food abundance. However, recent research has highlighted many neuro-behavioral and social aspects of obesity, with a suggestion that obesity, abdominal obesity in particular, may have evolved as a social signal. We tested here whether body proportions, and abdominal obesity in particular, are perceived as signals revealing personality traits. Faceless drawings of three male body forms namely lean, muscular and feminine, each with and without abdominal obesity were shown in a randomized order to a group of 222 respondents. A list of 30 different adjectives or short descriptions of personality traits was given to each respondent and they were asked to allocate the most appropriate figure to each of them independently. The traits included those directly related to physique, those related to nature, attitude and moral character and also those related to social status. For 29 out of the 30 adjectives people consistently attributed specific body forms. Based on common choices, the 30 traits could be clustered into distinct &#8216;personalities&#8217; which were strongly associated with particular body forms. A centrally obese figure was perceived as &#8220;lethargic, greedy, political, money-minded, selfish and rich&#8221;. The results show that body proportions are perceived to reflect personality traits and this raises the possibility that in addition to energy storage, social selection may have played some role in shaping the biology of obesity.</description>
      <guid>http://dx.doi.org/10.1038/npre.2008.2711.1</guid>
      <pubDate>Tue, 23 Dec 2008 16:59:39 UTC</pubDate>
      <dc:title>Obesity as a perceived social signal</dc:title>
      <dc:identifier>doi:10.1038/npre.2008.2711.1</dc:identifier>
      <dc:date>2008-12-23</dc:date>
      <dc:creator>Milind Watve</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-12-23T16:59:39Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Ecology</prism:section>
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      <title>Evolution of Thriftiness: An analytical viewpoint</title>
      <link>http://dx.doi.org/10.1038/npre.2008.2709.1</link>
      <description>We examine here, using a simple mathematical model, the conditions under which thrifty genes or fetal programming could evolve. Obesity and related disorders are thought to have their roots in metabolic thirftiness that evolved to combat periodic starvation. The failure to detect any thrifty genes and the association of low birth weight with type 2 diabetes, caused a shift in the concept from thrifty gene to thrifty phenotype and fetal programming. This hypothesis assumes that intra-uterine undernutrition programs the body to be thrifty, predicting and preparing for starvation in later life. However, there are reproductive costs associated with thriftiness. Results of the model suggest that under no condition thrifty and non-thrifty genes would co-exist stably in a population. The conditions for evolution of fetal programming are also very restricted. For species with longer life spans, programming for thriftiness is unlikely to evolve if starvation is decided by seasonality or stochastic annual climatic variations since the correlation between intra-uterine and life-time conditions is poor. On the other hand, if starvation is governed by longer periodicity factors such as population oscillations or social hierarchies, there can be better correlation between intra-uterine and life time conditions. Therefore social and population processes are more likely to have selected for fetal programming rather than seasonal and climatic &#8220;feast and famine&#8221; conditions. Since social and population processes can have cues other than diet, these cues may also influence the incidence of obesity related disorders as some recent evidence suggest.</description>
      <guid>http://dx.doi.org/10.1038/npre.2008.2709.1</guid>
      <pubDate>Tue, 23 Dec 2008 16:39:31 UTC</pubDate>
      <dc:title>Evolution of Thriftiness: An analytical viewpoint</dc:title>
      <dc:identifier>doi:10.1038/npre.2008.2709.1</dc:identifier>
      <dc:date>2008-12-23</dc:date>
      <dc:creator>Milind Watve</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-12-23T16:39:31Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
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      <title>Hypercytokinemia: Increased or decreased innate immunity?</title>
      <link>http://dx.doi.org/10.1038/npre.2008.2710.1</link>
      <description>The adipose tissue is an active endocrine organ which secretes proinflammatory cytokines and chemokines resulting into raised serum levels. Hypercytokinemia has been interpreted as raised level of innate immunity and its evolution is interpreted as a response to increased chances of infection under starvation conditions in which the thrifty phenotype evolved. If starvation and infection challenges co-occurred during hunter gatherer life, thrifty genotype and infection resistant genotype may have co-evolved. An inherent weakness of this explanation is that in obesity or insulin resistance there is no evidence of increased resistance to infections. The raised levels of inflammatory cytokines have not been demonstrated to combat infections or enhance wound healing. We suggest that the raised chemokine levels actually decrease peripheral innate immunity. The normal movement of monocyte-macrophages and neutrophils from blood vessels to injured tissue is under a chemokine gradient. A gradient results from the difference between the basal levels of chemokines and those secreted by the injured tissue. Increase in the basal level is expected to weaken the gradient thereby decreasing extravasation and infiltration. Using diffusion kinetics we show that a small rise in basal levels can cause substantial reduction in cell infiltration. This interpretation is consistent with the behavioural switch hypothesis proposed by Watve and Yajnik which suggests that obesity and insulin resistance mark a transition from &#8220;soldier&#8221; to &#8220;diplomat&#8221; lifestyle. Hypercytokinemia may have evolved as a mechanism of disinvestment in peripheral innate immunity since the diplomat lifestyle is less injury prone. We evaluate the two alternative hypotheses by available evidence.</description>
      <guid>http://dx.doi.org/10.1038/npre.2008.2710.1</guid>
      <pubDate>Tue, 23 Dec 2008 15:23:34 UTC</pubDate>
      <dc:title>Hypercytokinemia: Increased or decreased innate immunity?</dc:title>
      <dc:identifier>doi:10.1038/npre.2008.2710.1</dc:identifier>
      <dc:date>2008-12-23</dc:date>
      <dc:creator>Milind Watve</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-12-23T15:23:34Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Ecology</prism:section>
      <prism:section>Immunology</prism:section>
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      <title>Money handling influences BMI: a survey of cashiers</title>
      <link>http://dx.doi.org/10.1038/npre.2008.2708.1</link>
      <description>Money is a recent phenomenon in the evolutionary history of man and therefore no separate brain centre to handle money is likely to have evolved. The brain areas activated by food reward and money reward are extensively overlapping. In an experimental set-up, hunger was demonstrated to influence money related decisions and money related thoughts to influence hunger. This suggests that the brain areas evolved for handling food related emotions are exapted to handle money and therefore there could be a neuronal cross-talk between food and money. If this is true then attitude and behavior related to money and wealth could influence obesity. We conducted a survey of 211 individuals working as full time cashiers in order to test whether ownership over the cash, the amount of cash handled per day and the duration of cash handling work affected their body mass index (BMI).  Cashiers who had ownership over the money had a significantly higher age corrected mean BMI than salaried cashiers. The BMI correlated positively with duration of service as cashier even after correcting for age and duration of sedentary job in males. Among salaried cashiers of both sexes, bank cashiers whose mean daily cash handling was one or two orders of magnitude greater than that of shop cashiers, had a significantly higher BMI. The effects of amount of money handled per day, years of service as cashier and ownership over the money handled could be shown to influence BMI independent of each other. The results support the exaptation hypothesis and suggest that the changing economy and attitudes towards money may be a contributing factor to the current obesity epidemic.</description>
      <guid>http://dx.doi.org/10.1038/npre.2008.2708.1</guid>
      <pubDate>Mon, 22 Dec 2008 11:55:13 UTC</pubDate>
      <dc:title>Money handling influences BMI: a survey of cashiers</dc:title>
      <dc:identifier>doi:10.1038/npre.2008.2708.1</dc:identifier>
      <dc:date>2008-12-22</dc:date>
      <dc:creator>Milind Watve</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-12-22T11:55:13Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Ecology</prism:section>
      <prism:section>Neuroscience</prism:section>
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      <title>Caloric restriction causes symmetric cell division and delays aging in Escherichia coli</title>
      <link>http://precedings.nature.com/documents/2071/version/1</link>
      <description>Aging is one of the most intriguing processes of biology and despite decades of research, many aspects of aging are poorly understood. Aging is known to occur in bacteria and yeast that divide with morphological asymmetry. Morphologically symmetrically dividing bacteria such as Escherichia coli were assumed not to age until they were shown to divide with functional asymmetry leading to aging and death of some of the cells even in exponentially growing cultures. In asymmetrically dividing E. coli the newly synthesized components are presumed to occupy one pole so that after division one of the daughter cells receives newly synthesized components whereas the other retains the older components. Mathematical models predicted that at the population level, asymmetric growth should result in higher growth rate and symmetric growth in higher growth yield. Therefore, arguably symmetric cell division should be selected in low nutrient environments and asymmetric division in nutrient rich environments. A further prediction was that lower substrate concentrations should strengthen repair mechanisms and suppress aging whereas higher substrate concentrations suppress repair and enhance aging. We show here that E. coli divides more symmetrically under caloric restriction, that both genetic selection and phenotypic plasticity are important determinants of cell division symmetry and also that the proportion of cells that stop dividing and therefore are presumably dead is significantly lower in symmetrically dividing cultures. However, contrary to the prediction, symmetry was not always accompanied by reduced growth rate. These results demonstrate that asymmetry of division in E. coli is not hardwired but responsive to the nutritional environment. This provides a new perspective on why caloric restriction increases lifespan in organisms ranging from microbes to mammals. Symmetry of division may be a mechanism spanning across the width of life forms but regulating aging in different ways in different forms.</description>
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      <pubDate>Mon, 28 Jul 2008 14:55:40 UTC</pubDate>
      <dc:title>Caloric restriction causes symmetric cell division and delays aging in Escherichia coli</dc:title>
      <dc:identifier>hdl:10101/npre.2008.2071.1</dc:identifier>
      <dc:date>2008-07-28</dc:date>
      <dc:creator>Milind G. Watve</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-07-28T14:55:40Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Microbiology</prism:section>
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      <title>Sociobiological Control of Plasmid copy number</title>
      <link>http://dx.doi.org/10.1038/npre.2008.2016.1</link>
      <description>Background:All known mechanisms and genes responsible for the regulation of plasmid replication lie with the plasmid rather than the chromosome. It is possible therefore that there can be copy-up mutants. Copy-up mutants will have within host selective advantage. This would eventually result into instability of bacteria-plasmid association. In spite of this possibility low copy number plasmids appear to exist stably in host populations. We examined this paradox using a computer simulation model.Model:Our multilevel selection model assumes a wild type with tightly regulated replication to ensure low copy number. A mutant with slightly relaxed replication regulation can act as a &#8220;cheater&#8221; or &#8220;selfish&#8221; plasmid and can enjoy a greater within-host-fitness. However the host of a cheater plasmid has to pay a greater cost. As a result, in host level competition, host cell with low copy number plasmid has a greater fitness. Furthermore, another mutant that has lost the genes required for conjugation was introduced in the model. The non-conjugal mutant was assumed to undergo conjugal transfer in the presence of another conjugal plasmid in the host cell.Results:The simulatons showed that if the cost of carrying a plasmid was low, the copy-up mutant could drive the wild type to extinction or very low frequencies. Consequently, another mutant with a higher copy number could invade the first invader. This process could result into an increasing copy number. However above a certain copy number within-host selection was overcompensated by host level selection leading to a rock-paper-scissor (RPS) like situation. The RPS situation allowed the coexistence of high and low copy number plasmids. The non-conjugal &#8220;hypercheaters&#8221; could further arrest the copy numbers to a substantially lower level.Conclusions:These sociobiological interactions might explain the stability of copy numbers better than molecular mechanisms of replication regulation alone.  </description>
      <guid>http://dx.doi.org/10.1038/npre.2008.2016.1</guid>
      <pubDate>Thu, 26 Jun 2008 19:57:58 UTC</pubDate>
      <dc:title>Sociobiological Control of Plasmid copy number</dc:title>
      <dc:identifier>doi:10.1038/npre.2008.2016.1</dc:identifier>
      <dc:date>2008-06-26</dc:date>
      <dc:creator>Milind Watve</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-06-26T19:57:58Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Ecology</prism:section>
      <prism:section>Microbiology</prism:section>
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      <title>Streptomyces sp. as predators of bacteria</title>
      <link>http://dx.doi.org/10.1038/npre.2007.1263.2</link>
      <description>Background: The ecological role of actinomycetes and their secondary metabolites is not yet completely understood. Hypothesis: Actinomycetes and Streptomyces sp. in particular, are non-obligate predators of bacteria in soil. Evidence: Ability to grow on live bacterial cells as a sole source of nutrients. Prey cell lysis accompanying growth. Circumstantial evidence for the involvement of antimicrobials along with enzymes.Implications: This finding may open up a new source of novel secondary metabolites from the genus.</description>
      <guid>http://dx.doi.org/10.1038/npre.2007.1263.2</guid>
      <pubDate>Thu, 01 Nov 2007 17:00:03 UTC</pubDate>
      <dc:title>Streptomyces sp. as predators of bacteria</dc:title>
      <dc:identifier>doi:10.1038/npre.2007.1263.2</dc:identifier>
      <dc:date>2007-11-01</dc:date>
      <dc:creator>Milind G. Watve</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-11-01T17:00:03Z</prism:publicationDate>
      <prism:category>Presentation</prism:category>
      <prism:section>Biotechnology</prism:section>
      <prism:section>Ecology</prism:section>
      <prism:section>Microbiology</prism:section>
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