Pub Date : 2024-05-03eCollection Date: 2024-01-01DOI: 10.1093/emph/eoae007
Caleb E Finch
Senolytics are a new class of anti-aging drugs developed to selectively kill 'senescent' cells that are considered harmful in normal aging. More than 20 drug trials are ongoing with diverse 'senolytic cocktails'. This commentary on recent reviews of senolytics gives a historical context of mammalian cell senescence that enabled these new drugs. While cell senescence is considered harmful to aging tissues, many studies show its essential role in some regenerative and developmental processes for which senolytic drugs may interfere. Longer-term studies of side effects are needed before senolytics are considered for general clinical practice. The wide occurrence of cell senescence in eukaryotes, yeast to fish to humans, and suggests an ancient eukaryotic process that evolved multiple phenotypes.
{"title":"Senolytics and cell senescence: historical and evolutionary perspectives.","authors":"Caleb E Finch","doi":"10.1093/emph/eoae007","DOIUrl":"10.1093/emph/eoae007","url":null,"abstract":"<p><p>Senolytics are a new class of anti-aging drugs developed to selectively kill 'senescent' cells that are considered harmful in normal aging. More than 20 drug trials are ongoing with diverse 'senolytic cocktails'. This commentary on recent reviews of senolytics gives a historical context of mammalian cell senescence that enabled these new drugs. While cell senescence is considered harmful to aging tissues, many studies show its essential role in some regenerative and developmental processes for which senolytic drugs may interfere. Longer-term studies of side effects are needed before senolytics are considered for general clinical practice. The wide occurrence of cell senescence in eukaryotes, yeast to fish to humans, and suggests an ancient eukaryotic process that evolved multiple phenotypes.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"12 1","pages":"82-85"},"PeriodicalIF":3.7,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11097598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140956951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Improving the diversity and quality of genome assemblies for non-human mammals has been a long-standing goal of comparative genomics. The last year saw substantial progress towards this goal, including the release of genome alignments for 240 mammals and nearly half the primate order. These resources have increased our ability to identify evolutionarily constrained regions of the genome, and together strongly support the importance of these regions to biomedically relevant trait variation in humans. They also provide new strategies for identifying the genetic basis of changes unique to individual lineages, illustrating the value of evolutionary comparative approaches for understanding human health
{"title":"A multi-million-year natural experiment: comparative genomics on a massive scale and its implications for human health","authors":"Iker Rivas-González, Jenny Tung","doi":"10.1093/emph/eoae006","DOIUrl":"https://doi.org/10.1093/emph/eoae006","url":null,"abstract":"Improving the diversity and quality of genome assemblies for non-human mammals has been a long-standing goal of comparative genomics. The last year saw substantial progress towards this goal, including the release of genome alignments for 240 mammals and nearly half the primate order. These resources have increased our ability to identify evolutionarily constrained regions of the genome, and together strongly support the importance of these regions to biomedically relevant trait variation in humans. They also provide new strategies for identifying the genetic basis of changes unique to individual lineages, illustrating the value of evolutionary comparative approaches for understanding human health","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"32 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140575315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Here we introduce the EMPH special issue on Evolutionary and Biopsychosocial Perspectives on Sickness Communication. This Commentary provides an overview of each article and places them in the wider context of sickness as a social phenomenon with verbal and nonverbal signals. This Commentary, and the special issue in general, calls for greater attention to these signals that can affect pathogen transmission and may be at the evolutionary root of our caregiving systems and behaviors.
{"title":"Introduction to the Special Issue, Evolutionary and Biopsychosocial Perspectives on Sickness Communication","authors":"Eric C Shattuck, Chloe C Boyle","doi":"10.1093/emph/eoae005","DOIUrl":"https://doi.org/10.1093/emph/eoae005","url":null,"abstract":"Here we introduce the EMPH special issue on Evolutionary and Biopsychosocial Perspectives on Sickness Communication. This Commentary provides an overview of each article and places them in the wider context of sickness as a social phenomenon with verbal and nonverbal signals. This Commentary, and the special issue in general, calls for greater attention to these signals that can affect pathogen transmission and may be at the evolutionary root of our caregiving systems and behaviors.","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"20 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140316260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Absract Life history theory indicates that individuals/species with a slow pace of life invest more in acquired than innate immunity. Factors that decrease pace of life and predict greater investment in acquired immunity include increased nutritional resources, increased pathogen exposure and decreased risk of extrinsic mortality. Common care behaviours given to sick individuals produce exactly these effects: provisioning increases nutritional resources; hygiene assistance increases disease exposure of carers; and protection can reduce the risk of extrinsic mortality to sick individuals. This, study, therefore, investigated under what conditions care giving behaviours might impact immune strategy and pace of life. The study employed an agent-based model approach which simulated populations with varying levels of care giving, disease mortality, disease transmissibility, and extrinsic mortality, enabling measurements of how the immune strategy and age structure of the populations changed over evolutionary time. We used multiple regressions to examine the effects of these variables on immune strategy and the age structure of the population. The findings supported our predictions in that care selected for an acquired immunity. However, pace of life did not slow as expected. Instead, the population shifted to a faster, but also more cost intensive reproductive strategy in which care improved child survival by subsidizing the development of acquired immune responses.
{"title":"Could care giving have altered the evolution of human immune strategies?","authors":"Bethany L P Gilbert, Sharon E Kessler","doi":"10.1093/emph/eoae004","DOIUrl":"https://doi.org/10.1093/emph/eoae004","url":null,"abstract":"Absract Life history theory indicates that individuals/species with a slow pace of life invest more in acquired than innate immunity. Factors that decrease pace of life and predict greater investment in acquired immunity include increased nutritional resources, increased pathogen exposure and decreased risk of extrinsic mortality. Common care behaviours given to sick individuals produce exactly these effects: provisioning increases nutritional resources; hygiene assistance increases disease exposure of carers; and protection can reduce the risk of extrinsic mortality to sick individuals. This, study, therefore, investigated under what conditions care giving behaviours might impact immune strategy and pace of life. The study employed an agent-based model approach which simulated populations with varying levels of care giving, disease mortality, disease transmissibility, and extrinsic mortality, enabling measurements of how the immune strategy and age structure of the populations changed over evolutionary time. We used multiple regressions to examine the effects of these variables on immune strategy and the age structure of the population. The findings supported our predictions in that care selected for an acquired immunity. However, pace of life did not slow as expected. Instead, the population shifted to a faster, but also more cost intensive reproductive strategy in which care improved child survival by subsidizing the development of acquired immune responses.","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"85 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139584271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background/Objectives The concept of “demand” breastfeeding is central in public health. A key feature of the concept is that the infant is the locus of control in the breastfeeding process; when the breast is demanded by the infant, it is given the opportunity to feed. This study questions this notion of the infant as the locus of control in demand breastfeeding for empirical and theoretical reasons. From an evolutionary perspective, infants are expected to seek maximal investment and, against this backdrop of maximal investment-seeking, parents decide how much investment to put into offspring. Methodology Focal follows were conducted among 113 mother-infant dyads in Papua New Guinea. During these follows, response times and types of responses including breastfeeding to offspring fussing and crying were recorded. Results Infants were breastfed an average of 3.6 times/hour for just over 2 minutes/feed. Fussing and crying were responded to quickly, with most response times under 1 minute. When the mother responded, she breastfed the child approximately 52% of the time. The other 48% of the time, mothers responded to infants with other forms of pacification. Mothers were significantly less likely to respond to infants by breastfeeding if the child had been breastfed within the past 59-76 minutes. Conclusion/Implications As predicted by evolutionary parental investment theory, infants make frequent demands on their parents for investment, but mothers are ultimately the locus of control in the investment process. The mother decides whether and how frequently to breastfeed her offspring against this backdrop of near-continuous investment demands.
{"title":"Evolutionary and Empirical Perspectives on ‘Demand’ Breastfeeding: the Baby in the Driver’s Seat or the Back Seat?","authors":"David P Tracer","doi":"10.1093/emph/eoae003","DOIUrl":"https://doi.org/10.1093/emph/eoae003","url":null,"abstract":"Background/Objectives The concept of “demand” breastfeeding is central in public health. A key feature of the concept is that the infant is the locus of control in the breastfeeding process; when the breast is demanded by the infant, it is given the opportunity to feed. This study questions this notion of the infant as the locus of control in demand breastfeeding for empirical and theoretical reasons. From an evolutionary perspective, infants are expected to seek maximal investment and, against this backdrop of maximal investment-seeking, parents decide how much investment to put into offspring. Methodology Focal follows were conducted among 113 mother-infant dyads in Papua New Guinea. During these follows, response times and types of responses including breastfeeding to offspring fussing and crying were recorded. Results Infants were breastfed an average of 3.6 times/hour for just over 2 minutes/feed. Fussing and crying were responded to quickly, with most response times under 1 minute. When the mother responded, she breastfed the child approximately 52% of the time. The other 48% of the time, mothers responded to infants with other forms of pacification. Mothers were significantly less likely to respond to infants by breastfeeding if the child had been breastfed within the past 59-76 minutes. Conclusion/Implications As predicted by evolutionary parental investment theory, infants make frequent demands on their parents for investment, but mothers are ultimately the locus of control in the investment process. The mother decides whether and how frequently to breastfeed her offspring against this backdrop of near-continuous investment demands.","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"21 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139510457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In uncomplicated pregnancies, birthweight is inversely associated with adult non-communicable disease (NCD) risk. One proposed mechanism is maternal malnutrition during pregnancy. Another explanation is that shared genes link birthweight with NCDs. Both hypotheses are supported, but evolutionary perspectives address only the environmental pathway. We propose that genetic and environmental associations of birthweight with NCD risk reflect coordinated regulatory systems between mother and fetus, that evolved to reduce risks of obstructed labour. First, the fetus must tailor its growth to maternal metabolic signals, as it cannot predict the size of the birth canal from its own genome. Second, we predict that maternal alleles that promote placental nutrient supply have been selected to constrain fetal growth and gestation length when fetally expressed. Conversely, maternal alleles that increase birth canal size have been selected to promote fetal growth and gestation when fetally expressed. Evidence supports these hypotheses. These regulatory mechanisms may have undergone powerful selection as hominin neonates evolved larger size and encephalisation, since every mother is at risk of gestating a baby excessive for her pelvis. Our perspective can explain the inverse association of birthweight with NCD risk across most of the birthweight range: any constraint of birthweight, through plastic or genetic mechanisms, may reduce the capacity for homeostasis and increase NCD susceptibility. However, maternal obesity and diabetes can overwhelm this coordination system, challenging vaginal delivery while increasing offspring NCD risk. We argue that selection on viable vaginal delivery played an over-arching role in shaping the association of birthweight with NCD risk.
{"title":"Reconsidering the developmental origins of adult disease paradigm: the ‘metabolic coordination of childbirth’ hypothesis","authors":"Jonathan C K Wells, Gernot Desoye, David A Leon","doi":"10.1093/emph/eoae002","DOIUrl":"https://doi.org/10.1093/emph/eoae002","url":null,"abstract":"In uncomplicated pregnancies, birthweight is inversely associated with adult non-communicable disease (NCD) risk. One proposed mechanism is maternal malnutrition during pregnancy. Another explanation is that shared genes link birthweight with NCDs. Both hypotheses are supported, but evolutionary perspectives address only the environmental pathway. We propose that genetic and environmental associations of birthweight with NCD risk reflect coordinated regulatory systems between mother and fetus, that evolved to reduce risks of obstructed labour. First, the fetus must tailor its growth to maternal metabolic signals, as it cannot predict the size of the birth canal from its own genome. Second, we predict that maternal alleles that promote placental nutrient supply have been selected to constrain fetal growth and gestation length when fetally expressed. Conversely, maternal alleles that increase birth canal size have been selected to promote fetal growth and gestation when fetally expressed. Evidence supports these hypotheses. These regulatory mechanisms may have undergone powerful selection as hominin neonates evolved larger size and encephalisation, since every mother is at risk of gestating a baby excessive for her pelvis. Our perspective can explain the inverse association of birthweight with NCD risk across most of the birthweight range: any constraint of birthweight, through plastic or genetic mechanisms, may reduce the capacity for homeostasis and increase NCD susceptibility. However, maternal obesity and diabetes can overwhelm this coordination system, challenging vaginal delivery while increasing offspring NCD risk. We argue that selection on viable vaginal delivery played an over-arching role in shaping the association of birthweight with NCD risk.","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"52 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139506144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katherine R Amato, Priyanka Pradhan, Elizabeth K Mallott, Wesley Shirola, Amy Lu
Mammalian pregnancy is characterized by a well-known suite of physiological changes that support fetal growth and development, thereby positively affecting both maternal and offspring fitness. However, mothers also experience trade-offs between current and future maternal reproductive success, and maternal responses to these trade-offs can result in mother-offspring fitness conflicts. Knowledge of the mechanisms through which these trade-offs operate, as well as the contexts in which they operate, is critical for understanding the evolution of reproduction. Historically, hormonal changes during pregnancy have been thought to play a pivotal role in these conflicts since they directly and indirectly influence maternal metabolism, immunity, fetal growth, and other aspects of offspring development. However, recent research suggests the gut microbiota may also play an important role. Here, we create a foundation for exploring this role by constructing a mechanistic model linking changes in maternal hormones, immunity, and metabolism during pregnancy to changes in the gut microbiota. We posit that marked changes in hormones alter maternal gut microbiome composition and function both directly and indirectly via impacts on the immune system. The gut microbiota then feeds back to influence maternal immunity and metabolism. We posit that these dynamics are likely to be involved in mediating maternal and offspring fitness as well as trade-offs in different aspects of maternal and offspring health and fitness during pregnancy. We also predict that the interactions we describe are likely to vary across populations in response to maternal environments. Moving forward, empirical studies that combine microbial functional data and maternal physiological data with health and fitness outcomes for both mothers and infants will allow us to test the evolutionary and fitness implications of the gestational microbiota, enriching our understanding of the ecology and evolution of reproductive physiology.
{"title":"Host-gut microbiota interactions during pregnancy","authors":"Katherine R Amato, Priyanka Pradhan, Elizabeth K Mallott, Wesley Shirola, Amy Lu","doi":"10.1093/emph/eoae001","DOIUrl":"https://doi.org/10.1093/emph/eoae001","url":null,"abstract":"Mammalian pregnancy is characterized by a well-known suite of physiological changes that support fetal growth and development, thereby positively affecting both maternal and offspring fitness. However, mothers also experience trade-offs between current and future maternal reproductive success, and maternal responses to these trade-offs can result in mother-offspring fitness conflicts. Knowledge of the mechanisms through which these trade-offs operate, as well as the contexts in which they operate, is critical for understanding the evolution of reproduction. Historically, hormonal changes during pregnancy have been thought to play a pivotal role in these conflicts since they directly and indirectly influence maternal metabolism, immunity, fetal growth, and other aspects of offspring development. However, recent research suggests the gut microbiota may also play an important role. Here, we create a foundation for exploring this role by constructing a mechanistic model linking changes in maternal hormones, immunity, and metabolism during pregnancy to changes in the gut microbiota. We posit that marked changes in hormones alter maternal gut microbiome composition and function both directly and indirectly via impacts on the immune system. The gut microbiota then feeds back to influence maternal immunity and metabolism. We posit that these dynamics are likely to be involved in mediating maternal and offspring fitness as well as trade-offs in different aspects of maternal and offspring health and fitness during pregnancy. We also predict that the interactions we describe are likely to vary across populations in response to maternal environments. Moving forward, empirical studies that combine microbial functional data and maternal physiological data with health and fitness outcomes for both mothers and infants will allow us to test the evolutionary and fitness implications of the gestational microbiota, enriching our understanding of the ecology and evolution of reproductive physiology.","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"80 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139375627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background and Objectives Modern biocultural environments continue to place selective pressures on our skeletons. In the past century, a major cultural pressure has been the rise in sedentism. However, studies considering the effects of sedentism on the foot have largely considered pathological changes to the gross foot without particular regard for the pedal skeleton. To address this gap in the literature, temporal trends in the development of osteoarthritis and entheseal changes on the tarsals and metatarsals were analyzed in the context of biodemographic data for recent modern humans. Methodology The sample utilized for this project is comprised of 71 individuals from the William M. Bass Donated Skeletal Collection, with birth years ranging from 1909 to 1993. Temporal trends in osteoarthritis and entheseal changes were determined via ANCOVA, using year of birth as the explanatory variable and biodemographic variables (age, sex, stature, Body Mass Index, and tibial robusticity) as covariates. Results Results indicate that entheseal changes and osteoarthritis have decreased over time, and these trends are statistically significant. Temporal trends in pedal entheseal changes and osteoarthritis vary by sex. Conclusions and Implications The increase in sedentary behavior over time has usually been framed as a net negative for human health and well-being. However, considered in isolation, the decrease in entheseal changes and osteoarthritis presented here might be considered a positive development as they suggest overall less stress on the modern human foot. This study also has the potential to inform the health sciences and general public about biocultural contributors to modern foot health.
{"title":"Take a load off: Skeletal implications of sedentism in the feet of modern body donors","authors":"Malorie E Albee","doi":"10.1093/emph/eoad041","DOIUrl":"https://doi.org/10.1093/emph/eoad041","url":null,"abstract":"Background and Objectives Modern biocultural environments continue to place selective pressures on our skeletons. In the past century, a major cultural pressure has been the rise in sedentism. However, studies considering the effects of sedentism on the foot have largely considered pathological changes to the gross foot without particular regard for the pedal skeleton. To address this gap in the literature, temporal trends in the development of osteoarthritis and entheseal changes on the tarsals and metatarsals were analyzed in the context of biodemographic data for recent modern humans. Methodology The sample utilized for this project is comprised of 71 individuals from the William M. Bass Donated Skeletal Collection, with birth years ranging from 1909 to 1993. Temporal trends in osteoarthritis and entheseal changes were determined via ANCOVA, using year of birth as the explanatory variable and biodemographic variables (age, sex, stature, Body Mass Index, and tibial robusticity) as covariates. Results Results indicate that entheseal changes and osteoarthritis have decreased over time, and these trends are statistically significant. Temporal trends in pedal entheseal changes and osteoarthritis vary by sex. Conclusions and Implications The increase in sedentary behavior over time has usually been framed as a net negative for human health and well-being. However, considered in isolation, the decrease in entheseal changes and osteoarthritis presented here might be considered a positive development as they suggest overall less stress on the modern human foot. This study also has the potential to inform the health sciences and general public about biocultural contributors to modern foot health.","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"1 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139055182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jayasree Sengupta, Thomas Kroneis, Amy M Boddy, Rahul Roy, Anish Sarkar, Deepayan Sarkar, Debabrata Ghosh, Berthold Huppertz
The human embryo derives from fusion of oocyte and sperm, undergoes growth and differentiation, resulting in a blastocyst. To initiate implantation, the blastocyst hatches from the zona pellucida, allowing access from external inputs. Modelling of uterine sperm distribution indicates that 200-5000 sperm cells may reach the implantation-stage blastocyst following natural coitus. We show ultrastructural evidence of sperm cells intruding into trophectoderm cells of zona-free blastocysts obtained from the uterus of rhesus monkeys. Interaction between additional sperm and zona-free blastocyst could be an evolutionary feature yielding adaptive processes influencing the developmental fate of embryos. This process bears potential implications in pregnancy success, sperm competition, and human health
{"title":"Sperm intrusion into the implantation-stage blastocyst and its potential biological significance","authors":"Jayasree Sengupta, Thomas Kroneis, Amy M Boddy, Rahul Roy, Anish Sarkar, Deepayan Sarkar, Debabrata Ghosh, Berthold Huppertz","doi":"10.1093/emph/eoad043","DOIUrl":"https://doi.org/10.1093/emph/eoad043","url":null,"abstract":"The human embryo derives from fusion of oocyte and sperm, undergoes growth and differentiation, resulting in a blastocyst. To initiate implantation, the blastocyst hatches from the zona pellucida, allowing access from external inputs. Modelling of uterine sperm distribution indicates that 200-5000 sperm cells may reach the implantation-stage blastocyst following natural coitus. We show ultrastructural evidence of sperm cells intruding into trophectoderm cells of zona-free blastocysts obtained from the uterus of rhesus monkeys. Interaction between additional sperm and zona-free blastocyst could be an evolutionary feature yielding adaptive processes influencing the developmental fate of embryos. This process bears potential implications in pregnancy success, sperm competition, and human health","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"83 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139051358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-22eCollection Date: 2023-01-01DOI: 10.1093/emph/eoad042
Jibeom Choi
Cancer cells are highly cooperative in a nepotistic way and evolutionarily dynamic. Present cancer treatments often overlook these aspects, inducing the selection of resistant cancer cells and the corresponding relapse. As an alternative method of cancer elimination, autologous cell defection (ACD) was suggested by which modified cancer cells parasitically reliant on other cancer cells are implemented to the cancer cluster. Specifically, modified cancer cells should not produce costly growth factors that promote the growth of other cancer cells while receiving the benefit of exposure to such growth factors. Analytical models and rudimentary experiments up to date provide the medical feasibility of this method. In this study, I built comprehensive spatial simulation models by embracing the effects of the multiple growth factors, the Warburg effect, mutations and immunity. The simulation results based on planar spatial structures indicate that implementation of the defective modified tumours may replace the existing cancer cluster and defective cells would later collapse by themselves. Furthermore, I built a mathematical model that compares the fitness of the cells adjacent to the hypertumour-cancer interface. I also calculated whether anticancer drugs that reduce the effects of the growth factors promote or demote the utility of ACD under diverse fitness functions. The computational examination implies that anticancer drugs may impede the therapeutic effect of ACD when there is a strong concavity in the fitness function. The analysis results could work as a general guidance for effective ACD that may expand the paradigm of cancer treatment.
{"title":"Spatial simulation of autologous cell defection for cancer treatment.","authors":"Jibeom Choi","doi":"10.1093/emph/eoad042","DOIUrl":"https://doi.org/10.1093/emph/eoad042","url":null,"abstract":"<p><p>Cancer cells are highly cooperative in a nepotistic way and evolutionarily dynamic. Present cancer treatments often overlook these aspects, inducing the selection of resistant cancer cells and the corresponding relapse. As an alternative method of cancer elimination, autologous cell defection (ACD) was suggested by which modified cancer cells parasitically reliant on other cancer cells are implemented to the cancer cluster. Specifically, modified cancer cells should not produce costly growth factors that promote the growth of other cancer cells while receiving the benefit of exposure to such growth factors. Analytical models and rudimentary experiments up to date provide the medical feasibility of this method. In this study, I built comprehensive spatial simulation models by embracing the effects of the multiple growth factors, the Warburg effect, mutations and immunity. The simulation results based on planar spatial structures indicate that implementation of the defective modified tumours may replace the existing cancer cluster and defective cells would later collapse by themselves. Furthermore, I built a mathematical model that compares the fitness of the cells adjacent to the hypertumour-cancer interface. I also calculated whether anticancer drugs that reduce the effects of the growth factors promote or demote the utility of ACD under diverse fitness functions. The computational examination implies that anticancer drugs may impede the therapeutic effect of ACD when there is a strong concavity in the fitness function. The analysis results could work as a general guidance for effective ACD that may expand the paradigm of cancer treatment.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"461-471"},"PeriodicalIF":3.7,"publicationDate":"2023-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10727474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138801348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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