{
  "question": [
    "how does environment influence fertilisation",
    "how does diet impact someone's height",
    "which animal has the same number of chromosomes as human",
    "what's ensures brains work",
    "how do our brains maintain emotions"
  ],
  "answer": [
    "Environmental factors can influence fertilisation in several ways. Factors such as temperature, pressure, and chemical activity can affect the physiological processes involved in fertilisation. Lifestyle factors like smoking, irradiation, oral contraceptives, and low socioeconomic status can also impact natural conception. Moreover, environmental conditions can affect the quality of maternal care and offspring development. For instance, crowded larval environments can lead to a decline in quality over time, affecting the genetic polymorphism in populations. Additionally, environmental stressors can influence the responsiveness to prenatal stress, potentially affecting fertility.",
    "The text does not provide information on how diet impacts someone's height.",
    "The Bama miniature pig has the same number of chromosomes as humans.",
    "The functioning of the brain is ensured by the complex interplay of neuronal networks, synaptic connections, and the precise regulation of molecular and cellular events. This includes the spatiotemporal regulation of the transcriptome, the signaling dynamics of integrated circuitry, and the balance between activating and inhibiting systems. Additionally, the maintenance of genomic integrity in neuronal cells is crucial for the brain's high metabolic activity.",
    "Our brains maintain emotions through complex neural systems and processes. The reward-motivation system, which includes the striatum, amygdala, ventral tegmental area, orbitofrontal cortex, ventromedial prefrontal cortex, and anterior cingulate cortex, plays a key role in processing emotional and motivational information. The amygdala, a principal component of the limbic system, controls emotionality. Stress, anxiety, and other emotion-related traits are influenced by multiple genetic, environmental, experiential, and epigenetic factors. Additionally, hormones released by stressful experiences can enhance memory consolidation, further influencing emotional responses."
  ],
  "contexts": [
    [
      "This may be due to the cost of increased solicitation (reflected in reduced bodyweight for the effort expended) for which we found evidence in our study. Bodyweight is indeednegatively correlated with the level of offspring solicitation (GLM, F1,66 = 20.57, P < 0.001 e.g. day10, r = -0.39, and day 14, r = -0.44; Figure 6 and Supplementary file 2, e). DiscussionOur study of the genetics underlying family interactions has revealed that genes expressed in offspring can indirectly influence the quality of maternal behaviour and thus offspring fitness.",
      "UNINTENDED SELECTION IN LABORATORY ENVIRONMENTSIn nature, environmental variables are often highly correlated. For example, high-pressuredeep-sea habitats are generally cold, hydrothermal vents being an extremely rare (butextremely interesting) exception. The solubility of oxygen in water is negatively related totemperature; thus, even oxygen-saturated aquatic environments can have less availableoxygen than colder, subsaturated regions. In terrestrial environments, the saturatingvapor pressure of water increases dramatically with temperature, so that a parcel of aircontaining the same absolute quantity of water vapor will have a lower relative humidityas it warms.It hasalso been observed that, over the span of one generation, crowded larval environmentsshow a temporal decline in quality (Borash et al. 1998). Ammonia levels increase overtime, while food and ethanol levels decrease. This complexity appears to be responsiblefor a genetic polymorphism in crowded populations. Very early-developing genotypeshave high feeding rates but low tolerance to ammonia, while late-developing genotypesfeed more slowly and can tolerate higher ammonia levels. There may be many naturalenvironments that exhibit similar patterns of temporal decay (Borash et al. 1998).Temperature is the mostimportant and common physical variable affecting the distribution and abundance oforganisms in nature, as a 10C increase in temperature causes most biochemical reactions to increase in rate two- to threefold. Typical physiological temperatures span040C, although more extreme limits are well known (e.g. , overwintering plants andinsects, hot springs bacteria). Thus, selection experiments using temperature may behighly relevant to the real world. For aquatic organisms, the osmotic strength of the surrounding medium is an important environmental variable.In nature, thermodynamic variables such as temperature, pressure, and chemicalactivity (i.e. , the concentration of salts, hydrogen ions, etc. )differ across habitats. Lifeitself requires input of raw materials from the environment (nutrients, water, ions, etc. )that can then be used to drive physiological processes and make more organisms. We consider here two categories of environmental variables that have been used asselective agents in laboratory natural selection experiments.In ahumid environment, higher temperature will increase metabolism but wont increaseevaporative water loss; but in a dry environment, higher temperatures will increasemetabolism and water loss. A call for greater ecological realism is not without precedent. Ecologists have developed sophisticated laboratory facilities that can mimic simple terrestrial ecosystems. AtSilwood Park, for instance, the Ecotron consists of fifteen environmental chambers ableto control and manipulate photoperiod, illumination (balanced spectrum, dawn/dusksimulation), temperature, humidity, rainfall, and even CO2 (Lawton 1996). The chambers house multispecies ecosystems, allowing for complex ecological interactions ofplants and animals.",
      "Alternatively, the \"limited oocyte pool\" hypothesis (Warburton, 1989) suggests a more direct effect of antral oocyte pool size on the risk of aneuploidy.The limited number of antral follicles available in older women could lead to the selection of a suboptimal oocyte for ovulation, for example one that is either immature or postmature.Some experimental evidence in other mammals supports the idea that such Sample described in Warburton et al. (1986).",
      "In the most general terms, three types of environmental factors can influence human health during aging: physical, chemical, and biological.Physical factors include temperature and solar radiation.Chemical factors from natural and biological sources include trace toxins (asbestos, lead, tobacco smoke), but also trace morphogens that can cause subtle abnormalities in development.Biological factors include diet and infectious organisms, but also stress from social interactions.We know little about the concentrations of a vast number of bioactive substances that may be present sporadically in the environment.It seems fair to say that our concept of the environment will evolve rapidly with new technical developments and may come to include multigenerational effects.For example, in the case of diabetes, the maternal physiological state existing before pregnancy can influence fetal growth.Moreover, the ovary acquires its full stock of eggs in the fetus: thus, the egg cell from which all of our cells stem was exposed to the environment of our maternal grandmother (Finch and Loehlin, 1998).The depth of the transgenerational environment is a completely obscure aspect of human experience.",
      "Low human fertilityAnother area of interest is that of changing fertility patterns in the developed world.Currently ESRC investment is focused upon both the economic and social trajectories of demographic change.There are a number of significant questions that need to be addressed in relation to involuntary infertility however.For example, infertility rates, which appear to be rising, and also the considerable variation that exists in the timing of the ending of the human reproductive span.Researchers need to know whether these factors are genetic, gene/environment interactions, or entirely environmentally induced, and why there is a need for heterogeneity of fecundity in biometric models of fertility, coital frequency or genetics (Hobcraft, 2003).",
      "UNINTENDED SELECTION IN LABORATORY ENVIRONMENTSIn nature, environmental variables are often highly correlated. For example, high-pressuredeep-sea habitats are generally cold, hydrothermal vents being an extremely rare (butextremely interesting) exception. The solubility of oxygen in water is negatively related totemperature; thus, even oxygen-saturated aquatic environments can have less availableoxygen than colder, subsaturated regions. In terrestrial environments, the saturatingvapor pressure of water increases dramatically with temperature, so that a parcel of aircontaining the same absolute quantity of water vapor will have a lower relative humidityas it warms.It hasalso been observed that, over the span of one generation, crowded larval environmentsshow a temporal decline in quality (Borash et al. 1998). Ammonia levels increase overtime, while food and ethanol levels decrease. This complexity appears to be responsiblefor a genetic polymorphism in crowded populations. Very early-developing genotypeshave high feeding rates but low tolerance to ammonia, while late-developing genotypesfeed more slowly and can tolerate higher ammonia levels. There may be many naturalenvironments that exhibit similar patterns of temporal decay (Borash et al. 1998).Temperature is the mostimportant and common physical variable affecting the distribution and abundance oforganisms in nature, as a 10C increase in temperature causes most biochemical reactions to increase in rate two- to threefold. Typical physiological temperatures span040C, although more extreme limits are well known (e.g. , overwintering plants andinsects, hot springs bacteria). Thus, selection experiments using temperature may behighly relevant to the real world. For aquatic organisms, the osmotic strength of the surrounding medium is an important environmental variable.In nature, thermodynamic variables such as temperature, pressure, and chemicalactivity (i.e. , the concentration of salts, hydrogen ions, etc. )differ across habitats. Lifeitself requires input of raw materials from the environment (nutrients, water, ions, etc. )that can then be used to drive physiological processes and make more organisms. We consider here two categories of environmental variables that have been used asselective agents in laboratory natural selection experiments.In ahumid environment, higher temperature will increase metabolism but wont increaseevaporative water loss; but in a dry environment, higher temperatures will increasemetabolism and water loss. A call for greater ecological realism is not without precedent. Ecologists have developed sophisticated laboratory facilities that can mimic simple terrestrial ecosystems. AtSilwood Park, for instance, the Ecotron consists of fifteen environmental chambers ableto control and manipulate photoperiod, illumination (balanced spectrum, dawn/dusksimulation), temperature, humidity, rainfall, and even CO2 (Lawton 1996). The chambers house multispecies ecosystems, allowing for complex ecological interactions ofplants and animals.",
      "How do we improve reproductive success and reduce the effects of maternal aging in the natural population as well as in the clinic?Identification of lifestyle factors that affect natural conception is important.Several factors including smoking, irradiation, oral contraceptives and low socioeconomic status (Christianson et al., 2004;Hunter et al., 2013) have been implicated but their molecular basis has yet to be elucidated.Disentangling the factors that influence aneuploidy may provide us with lifestyle interventions to reduce miscarriage rates and may move the J curve to the right and prevent the early truncation of reproductive lifespan caused by aneuploidy.",
      "Several lines of evidence further suggest that fetal genetic effects may influence birth timing.First, fetal genes that are paternally imprinted mainly control placental and fetal membrane growth [16] .Because the placenta and fetal membranes likely play a role in preterm birth, fetal genes controlling these tissues may also contribute.Additionally, a study comparing the correlation in gestational age between full and half siblings suggests that preterm birth is influenced in part by fetal genetic factors [15] .Lastly, several studies suggest that paternity affects risk for the disorder.For example, several studies indicate that partner changes between pregnancies reduced risk of preterm birth [17,18] ; however, changes in paternity may reflect association with long interpregnancy intervals rather than paternity effects per se.Paternal race also has been associated with preterm birth risk.Previous studies observed that preterm birth rates are highest when both parents are Black and remain higher when one parent is Black, whether that parent is the mother or father [19,20] , suggesting that fetal race also influences birth timing.However, father's family history of preterm birth has been shown to have only a weak association with risk.While an early study of a Norwegian birth registry demonstrated a correlation between father and children's gestational ages [21] , a more recent and extensive study of this registry suggested fathers contributed little to no risk to preterm delivery [22] .Similarly, a recent study [14] suggested that paternal genetics contributed little to gestational age, but could not refute the possible role of maternally-inherited genes expressed in the fetus.Hence, while paternally-in-herited genes may contribute little to preterm birth or other disorders, maternally-inherited genes expressed in the fetus may still be important.Together, these data suggests that the fetal genome may contribute to birth timing, motivating further study defining the infant as the proband.",
      "Young maternal age at conception may play a role in longer child telomere length but again the biology of these relationships including environmental versus genetic factors need to be better studied (Prescott et al. 2012).Furthermore, as rate of change reflects both genetic and environmental influences, it is important to determine whether parental rate of change might covary with child rate of change.",
      "6.2 Mechanisms of indirect genetic effects on maternal care6.2.1 Prenatal effectsOffspring effects on maternal investment and postnatal behaviour begin in utero. Theplacenta is vital for the development of offspring in eutherian mammals (John and Surani,2000) by regulating transfer of nutrients from mother to offspring (Constncia et al. , 2002),which in turn increases maternal food intake (Newbern and Freemark, 2011) and alsoprimes the maternal brain for parenting behaviour (Bridges et al. , 1990, 1997).",
      "DISCUSSIONDespite the fact that genetic factors that reduce the ability of an individual to reproduce are expected to be under intensive negative selection, reduced fertility is a common health condition in humans (de Kretser, 1997;Agarwal et al., 2015) and an important economic trait in dairy cattle.Previous studies that included measurements of progesterone and pregnancy-specific protein B levels suggested that a large portion of recorded non-conceptions in human and cattle are apparently the result of unrecognized EA (Edmonds et al., 1982;Humblot, 2001;Santos et al., 2004;Carthy et al., 2015).Markers are sorted in descending order of the probability to reject the null hypothesis of no effect on putative early abortion rate.The substitution effects and coefficients of determination are given for each marker for putative early abortion and conception status.",
      "by the gross limitations of forward genetic approaches in humans,including limited ability to dissect environmental factors and gene XWhat this study addsenvironment interactions, particularly the contribution of environmen- Identifies candidate genes that may moderate the effectstal factors in utero (Burmeister, McInnis, & Zllner, 2008; Henriksen,of prenatal stress on cocaine responsiveness. Nordgaard, & Jansson, 2017), and these limitations in turn hinder the Demonstrates sex as a factor that moderates the effectsdevelopment of a mechanistic understanding of aetiology. Here, weof early life stress on cocaine responsiveness."
    ],
    [
      "Year Period, lbsNote.Weight changes are shown per increase in daily serving of the food or beverage.All weight changes were adjusted simultaneously for age, baseline body mass index, sleep duration, smoking status, physical activity, television watching, alcohol use, and all the dietary factors shown.Source.Adapted from Mozaffarian et al.6Women who increased their adherence to a Western pattern (high intakes of red and processed meats, refined grains, sweets or desserts, SSBs, and potatoes) gained the most weight across 8 years of follow-up.In parallel, women who increased their adherence to a prudent pattern (high intakes of fruits, vegetables, whole grains, fish, poultry, and salad dressing) gained the least weight. 14n a recent study of dietary quality characterized by established healthy diet indices (i.e., a Mediterranean-style diet, the Alternate Healthy Eating Index, and the Dietary Approaches to Stop Hypertension diet), higher or increasing adherence to any of these indices was associated with less weight gain in a given 4-year interval through midlife, with greater benefits observed in overweight women.15 (For additional information on dietary assessments in the NHS, please see Hu et al. in",
      "In onestudy, vitamin D levels were inversely correlated with BMI(r = -0.22, p = 0.025), suggesting some potential benefitsfor individuals living with obesity, although this remainsto be investigated in a prospective study.14 For individuals living with obesity, an eight-week low-calorie dietprogramme supplemented with vitamin D led to a significant decrease in inflammatory markers, compared withthe same diet with a placebo supplement.15 Obesity isassociated with low plasma levels of 25-hydroxy-vitaminD, which can result from vitamin D deficiency.1619 Therefore, we compared body weights of the mice from eachgroup before and after treatment.",
      "In all study cohorts, height and weight were measured wearing light clothing and no shoes, and BMI was calculated as weight divided by the square of the height (kg/m 2 ).Written informed consent was obtained from all participants and the research protocol was approved by the local human research ethics committees.",
      "age-adjusted height residuals, cm.",
      "explained by genes predisposing to obesity.The National Academy of Sciences-National Research Council (NAS-NRC) World War (WW) II Veteran Twin Registry of White male twin pairs 5 had their height, weight, and BP measured at the induction physical examination, which offers a unique opportunity to investigate the following questions: (1) the relative influence of genetic and environmental factors on height, weight, BMI, and BP (SBP and DBP); (2) the extent to which genetic and environmental influences on SBP and DBP are shared with those influencing BMI; (3) whether BMI has any modifying effect on genetic and environmental influences on SBP and DBP.What Is New?  In the largest twin cohort with measured (rather than self-reported) weight, height, and blood pressure (BP), we investigated (1) the relative influence of genetic and environmental factors on height, weight, body mass index (BMI), and BP (systolic BP [SBP] and diastolic BP [DBP]); (2)  the extent to which genetic and environmental influences on SBP and DBP are shared with those influencing BMI; (3) whether BMI has any modifying effect on genetic and environmental influences on SBP and DBP.",
      "Over the last few decades, the adoption in Asian populations of western-style diets of increased fats and carbohydrates and of more sedentary habits has led to a marked increase in obesity (23,24).In particular, a cohort of women from the ongoing Cebu Longitudinal Health and Nutrition Survey (CLHNS) based in the Philippines showed a sixfold increase in prevalence of overweight and obesity associated with nearly two decades of substantial and continuing socioeconomic modernization (also illustrated by an increase in mean weight of 6.8  7.1 kg) (24).The portion of increased prevalence due to the changes in environment vs. increased age of these women is unclear.",
      "In onestudy, vitamin D levels were inversely correlated with BMI(r = -0.22, p = 0.025), suggesting some potential benefitsfor individuals living with obesity, although this remainsto be investigated in a prospective study.14 For individuals living with obesity, an eight-week low-calorie dietprogramme supplemented with vitamin D led to a significant decrease in inflammatory markers, compared withthe same diet with a placebo supplement.15 Obesity isassociated with low plasma levels of 25-hydroxy-vitaminD, which can result from vitamin D deficiency.1619 Therefore, we compared body weights of the mice from eachgroup before and after treatment.",
      "ResultsTable 2 displays anthropometric, biochemical and dietary characteristics of the study sample.The sample included 288 men and 383 women, with a mean age of 40.59 8 14.79 years.The individuals were on average overweight (BMI = 27.75 8 7.63) and their dietary fat intake represented 34.3% of daily energy intake.The results of significant interactions (p value ^ 0.01) are presented in table 3 and suggest that the majority of the SNPs that have been initially associated with T2DM at high levels of statistical significance in GWAS reports did not interact with dietary fat intake to influence either adiposity-or glucose homeostasis-related phenotypes.",
      "Child weight parameters and accelerated shortening in childhoodObesity at different points in early childhood did not correlate with the rate of telomere attrition from 4 to 5 years of age (Table 4).Similarly, abdominal obesity did not correlate with the rate of telomere attrition (p = 0.65) (Table 4).",
      "Diet significantly alters lifespan, not weight gain per seAuthor ManuscriptWe chose to focus on two time points for body weight analyses100 days on diet as a pointto evaluate early weight gain on HFD, and 400 days on diet, a stage that is close to themaximal weight on both diets. The mean weight of the population plateaus around 500 daysof age and declines thereafter on both diets.The consensus model highlighted a potential causal effect of diet on peak bodyweight measured relatively late in life (500 days), acting through circulating levels of totalNat Metab. Author manuscript; available in PMC 2022 March 22. Roy et al. Page 7Author Manuscriptand high-density lipoprotein cholesterol measured in the old-aged group (Extended Figure2). The Bayesian network analysis, as we structured it, failed to show any causality betweenserum metabolites and variability in lifespan.Early body weight gain associated with reduction in lifespanBody weight measured after 100 days on both diets also correlates negatively with lifespan,after adjusting for strain differences (Figure 3C), a one-gram increase now corresponding toa decrease of 4 days (p<0.0001, r = 0.22). Looking at change in body weight after 100 dayson diet, early body weight gain in response to HFD, but not CD, trended to be negativelycorrelated with lifespan, with a one-gram gain corresponding to a decrease of ~1.5 days (p =0.08, r = 0.06) (Figure 3D).(E) After 400 days on diet (~500 days age), body weight does not predictvariance in lifespan (see line labeled d in Panel A) (p = 0.63, r = 0.01) (n = 447 on CDand HFD). (F) Substantial weight change after prolonged HFD feedingdifference frombaseline to 400 days on diet (blue line)does not predict lifespan (p = 0.26, r = 0.02). (G)Strain-wise changes in median weight after 100 days on diets. Red points represent lifespansof cases on CD and blue points those on HFD. Lines represent median body weight (lefty axis).(C) Body weight after 100 dayson both diets (~260 days age) correlates negatively with lifespan (4 days/g, p <0.001, r =0.3, see line labeled c in Panel A) (n = 626 on CD, 665 on HFD). (D) Early weight changein response to HFD (blue line)the difference from baseline after 100 days on dietwasnegatively related with lifespan (4 days/g, p = 0.004, r = 0.1), but this is not true of casesremaining on CD.",
      "Her father was 170 cm in height and grew significantly at the age of 14 years.Her mother was 153 cm in height with menarche at the age of 13 years.Her younger brother was 6 years old and maintained a height above the 50th percentile of the population with the same age and gender.There was no family history of diabetes mellitus or short stature.Her father is 172 cm, grew significantly at the age 15 years.Her mother is 158 cm and had menarche at age 14 years.Her elder brother is 22 years old and his height is 180 cm.There is no family history of diabetes mellitus or short stature.",
      "Adult height is the result of both growth throughout childhood and loss of height during the aging process.We therefore assessed the influence of age on the 20 robust associations.We did not find any evidence that the effects on height were different in individuals o50 years compared to those aged 450 years (all P 4 0.01; similar results were obtained when we used a cut-off of 40 years of age), or when adjusting for age decade (see Supplementary Table 4 online).This suggests that the effects are predominantly on developmental and childhood growth rather than on processes involved in loss of height, although studies of more young adults and children are needed to confirm this.",
      "IntroductionHeight, fat mass, and fat distribution differ substantially between men and women, and these differences may, in part, explain the sex-specific susceptibilities to certain diseases [1,2].A subtle sexual dimorphism in body composition is already apparent during childhood, and emerges more prominently during adolescence as boys start exceeding girls with regard to height and muscle mass, while girls accumulate more fat mass [3][4][5].These considerable differences in anthropometry may reflect sex-specific differences in steroid hormone regulation, adipogenesis, lipid storage, muscle metabolism, composition, and contractile speed, skeletal growth and maturation, or lipolysis, and suggest a genetic underpinning [1,2,[6][7][8][9][10]."
    ],
    [
      "To facilitate comparative research, the Alliance of GenomeResources provides an interface that allows users to searchfor and view genes, functional data, and disease associations from databases of the fly, mouse, rat, yeast, nematode,and zebra fish (http://www.alliancegenome.org, last access:3 January 2018). 3The mouse as a model animal for livestockresearchMice are mammals, sharing 92 to 95 % of protein coding genes with humans and other mammalian livestockspecies, such as cattle (Elsik et al. , 2009), pigs (Humphrayet al. , 2007), sheep (Iannuzzi et al. , 1999), and goats(Schibler et al. , 1998).",
      "Sex ChromosomesSeveral studies have revealed high degrees of homology among autosomal chromosomes of bovids with similar banding patterns and gene order among the chromosome arms of cattle, river buffalo, sheep, and goats [14,15].Bovid sex chromosomes, unlike the highly similar autosomal chromosomes, share a slightly more complex rearrangement of sequences [5].Chromosome banding comparisons show that while large portions of these chromosomes are conserved, BBU-X has large blocks of constitutive heterochromatin that BTA-X lacks.Cytogenetic studies representing loci order on these sex chromosomes show complex rearrangements that may have occurred during the karyotype evolution of river buffalo and cattle.BBU-X and BTA-X share the same gene order but a different centromere position, indicating a centromere translocation event with the loss of constitutive heterochromatin in BTA-X, which differentiates it from BBU-X [5].Comparative FISH mapping shows the existence of a similar situation in river buffalo and cattle Y-chromosomes.BTA-Y and BBU-Y differ in an inversion including the centromere and breakage points in both arms (pericentric inversion) where BBU-Y is larger than BTA-Y and gains heterochromatin [5].Figure 1: At the cytogenetic level, water buffalo chromosomes can be matched to bovine chromosomes arm for arm.Each biarmed water buffalo chromosome is derived from the fusion of two bovine acrocentrics. (a) This shows the similar banding patterns for bovine chromosomes 29 and 16 to water buffalo chromosome 5 [22], (b) This shows similar banding patterns for bovine chromosome 12 and water buffalo chromosome 13 [22].",
      "Second,it is possible to replicate experiments in reference cohorts (also known as referencepanels or reference populations), which is impossible in humans except for in cases ofmonozygotic twins. Third, it is easy to control the environment and model geneenvironment (GXE) interactions in mice [75]. Fourth, despite strong functional effects,the minor allele frequencies are often too low in the human population to attain sufficientstatistical power and significance in large association studies. In contrast, most of murinecrosses have been derived from two inbred strains, and as a result allele frequencies areclose to 0.5.",
      "Figure S3.Chromosome karyotype of Bama miniature pig, Related to Figure 3. (A) Male and (B) Female.The examination of karyotype of Bama miniature pig by means of peripheral blood lymphocytes culture showed that the diploid chromosomes number was 38, 18 pairs of autosomes and one pair of sex chromosomes in both males (XY) and females (XX).The chromosomes were divided into four groups of a, b, c and d according to the standard of Reading Congress.The karyotype of the autosomes was 10sm+4st+10m+12t.The X chromosome was a metacentric chromosome whose length was between the 8 th and 9 th chromosome, while the Y chromosome was the smallest metacentric chromosome.Comparison of the BM genome with the human, and three common experimental animal (macaque, mouse, and dog), genomes unveiled three gene families, including ARF1 and IGHD, shared between the BM and human genomes but absent in macaque, mouse, and dog genomes (Figure S10).These genes may play roles in Alzheimer disease, pituitary dwarfism, and growth failure (from database ''Dis-GeNET'').The presence of these genes in the BM potentially facilitates research on the abovementioned diseases using this animal model.Moreover, BM has fewer unique genes compared with the Duroc (1,303 versus 1,531) (Figure S10), and the genes specific to BM were significantly enriched in the ''steroid hormone biosynthesis'' Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway (p = 0.00908), which is associated with sex hormone secretion, male testicles development, and rapid maturation of sperm.",
      "Mice are evolutionarily relatively close to humans, and their size and short generationtime allows experiments to be set up and run with large enough numbers for statistical signicance. However, other types of model organisms such as zebrash[206] and worm[176] can oer unique advantagesover using rodents. While these organisms have a larger evolutionarydistance to humans, they are cheaper, faster and easier to breed and281.4. BIOINFORMATIC OPPORTUNITIEShave transparent bodies that are easy to dissect.[226]have shown that the conservation level between C. elegans and manis sucient to infer gene-gene interactions in man from worm data. Even though the global disease phenotypes may not be at all comparable, the molecular basis may be common (e.g. breast cancer andhigh male incidence of progeny). For example, research on stress response in C. elegans has provided detailed insight into the genetic andmolecular mechanisms underlying complex human diseases [294].",
      "Even within mammals, where SrYis the gene responsible for testis determination,monotremata show a different multichromosomal sex determination mechanism (involving5X + 5Y chromosomes), and recently, threespecies in the rodent line have demonstrateda different switching gene to SrY (Graves andPeichel, 2010). The high conservation of sexdetermination within birds and mammals hasprobably to do with their high developmentFunctional Genomic Analysis of Sex Determination and Differentiation in Teleost Fishhomeostasis, including constant body temperature (Barske and Capel, 2008).",
      "Drosophila melanogaster 240Xenopus laevis 600",
      "Based on the branch-length valuesin Figure 6.1, a comparison of man and mouse has D = 0.63, but adding rat as athird species increases total D to 0.72. When calculating total D for an analysis, eachunique section of branch is counted only once, so rat adds only D = 0.086 to thetotal analysis; considerably more power could be added by using dog instead of, or inaddition to rat, as it would contribute D = 0.244 of unique branch length.",
      "5C), being shared with ve other vertebrates,including dog (XM_848628), horse (XM_001916545), cow(NM_001099130), chimpanzee (XM_001150577), and human(NM_002202). This is also true of wild-derived subspecies andspecies of Mus, including Mus musculus musculus, Mus musculuscastaneus, and Mus spretus, which have also been sequenced aspart of the Mouse Genome Project. In marked contrast, 14 otherstrains of mice have the less conserved B allele. This suggeststhat the E-box is a regulatory element now widely propagated ina subset of laboratory mice, including B6/J.",
      "Animal models have been widely used to study topicsthat could not be easily studied using human populations. In particular, rodent models such as those in mice havecontributed tremendously to our understanding of humangenetics and genomics. We will examine the sex similarityand dierence using data of whole genome gene expressionproles from a well-known mouse population of recombinant inbred (RI) strains derived from C57BL/6J andDBA/2J (BXD), which is the largest RI mouse populationand with remarkable data on whole genome expressionproles and phenotypes [1618].",
      "They arenot more complex than mice or more deeply thoughtful than dogsor pigs, but they are incontrovertibly more similar biologically tohumans. This in itself is a reason for using these species in researchdespite the cost and emotional qualms their use engenders. A vocal wing of the legal community, led by Steven Wise,Laurence Tribe, and Alan Dershowitz, is exploring the idea thathumanity quotients can be assigned to life forms as diverse ashoneybees and chimpanzees, arguing that each species should beprovided with scaled legal protection.This scaling applies evento an organ such as brain that is considered unusually large inhumans; the brains of both mice and humans comprise roughly2% of total body mass, and in terms of neuron numbers mice areactually proportionally brainier than humans (approx 75 millionvs 100 billion neurons). Like humans, mice have significant bodysize sexual dimorphism; males typically weigh 3050% more thanfemales. The main advantage of small size is that a set of 810 animalscan be maintained in good health in a shoebox-sized cage.",
      "Marsupial Sex Chromosomes and Sex DeterminationComparative sequencing, gene mapping, and chromosome painting between marsupials and eutherians, along with comparison with a chicken out-group, have revealed that the human X chromosome is made up of two ancient gene blocks, both of which are autosomal in chickens (Figure 6).One block, representing the marsupial X, is shared with approximately two-thirds of the eutherian X.A second block is also autosomal in marsupials and so must represent a region added to the X in a eutherian ancestor (44).Mapping the same genes in elephants shows that the fusion point of the ancient and added region corresponds to the centromere (109), suggesting an original Robertsonian fusion 160-105 Mya followed by a centric shift in the ancestor of non-afrotherian lineages.The lack of homology between the mammal XY and bird ZW sex chromosomes (81) and between the mammal XY and the varied systems of reptiles, frogs, and fish implies that the mammal XY system (and the SRY gene) arose later than 310 Mya (46).A much later date emerged from the surprising findings that the two gene blocks that make up the human XY pair are both autosomal in monotremes (platypus and echidna) and that the monotreme XY complex has homology instead to the bird ZW (133).This dates the emergence of the therian sex chromosomes and SRY at 166-160 Mya.Marsupials, like eutherians, normally have an XX female:XY male chromosomal sex determination or some simple variant [X 1 X 2 Y and XY 1 Y 2 systems, in which an autosome has become fused to the X or Y chromosome, are quite common in marsupials (49)].The X chromosome is smaller than the highly conserved 5% of the eutherian genome, and the basic Y chromosome is minute.The X and Y chromosomes do not undergo homologous pairing over a pseudoautosomal region in marsupials, which is a requirement for fertility in mice and humans.Instead, pairing makes use of a proteinaceous basal plate to which the X and Y are attached during meiosis and from which they segregate (33).",
      "Based on the branch-length valuesin Figure 6.1, a comparison of man and mouse has D = 0.63, but adding rat as athird species increases total D to 0.72. When calculating total D for an analysis, eachunique section of branch is counted only once, so rat adds only D = 0.086 to thetotal analysis; considerably more power could be added by using dog instead of, or inaddition to rat, as it would contribute D = 0.244 of unique branch length.",
      "Taking the most conservative estimate, Comparison of genome wide studies in vertebrates and flies"
    ],
    [
      "The neuronal networks formed by this largenumber of massively interconnected neurons generate complex spatiotemporal patterns ofneuronal activity that require coordinated activity across large populations of neurons usingboth short- and long-range synaptic connections. On an even larger scale, the mammalianbrain is composed of many structurally diverse networks, including the neocortex, thalamus,basal ganglia etc. Healthy brains are characterized by the continuous generation of behaviorrelated spatiotemporal activity patterns that propagate across multiple brain areas.",
      "To retaingenes that are more active when the brain is still undergoing corematurational processes in humans, we used BrainSpan to select autosomaltranscripts expressed at least 1.5-fold more during the early postnataldevelopment (018 months after birth) than in adulthood (2040 years ofage), with the nal networks consisting of 154 genes in the PFC (seeTable S4) and 72 genes in the NAcc (see Table S5).",
      "Heath: Do you have a hypothesized mechanism by which you get from earlyseparation to altered response when you are genetically vulnerable? Battaglia: Yes, one mechanism might have to do with the cholinergic system:intense stress causes some alternative splicing of acetylcholine esterase (Kaufer etal 1998). This has been found to be protective for the brain. One of our hypotheseshowever is that the same mechanism which may be protective for the higher braincan be a risk factor for the lower brain, for instance the medulla, because it mayenhance sensitivity to suffocatory stimuli (Battaglia & Ogliari 2005).",
      "The rapidly expanding set of inference engines currently has 5 interrelated modules: BrainParts (gray matter regions, major fiber tracts, and ventricles),Cell Types, Molecules, Connections (between regions and celltypes), and Relations (between parts identified different neuroanatomical atlases). Nature Precedings : doi:10.1038/npre.2009.4000.1 : Posted 23 Nov 2009A genome-wide, 3-dimensional map of gene expression inthe adult mouse brain, the ABA reveals the expression patterns of approximately 20 000 genes throughout the adultmouse brain to the cellular level.",
      "Furthermore, it was suggested that thebrain is prone to hyperactivity, and this hyperactive tone is down-regulated by brainregions and neurotransmitter systems that decrease the PA (Rowland 1998; Viggiano2008). It was proposed that the reticular activating system is responsible for arousalwhile cerebral cortex is mostly inhibitory (Rowland 1998). All in all, the interplay ofthe activating and inhibiting systems serves the purpose of maintaining so calledsensoristasis (term created by Schultz in 1965) which is an optimal level of sensorystimulation of the nervous system for each individual (Rowland 1998).",
      "In the brain, more than any other organ, function followsform, he says. Cellular resolution of expression patterns will provenecessary to uncover as yet unknown relationships betweencircuitry, cell type, and gene expression in the brain, saysArthur Toga, a neuroscientist at the University of California,Los Angeles, and Allen Brain Atlas advisor. Ed Lein, aneuroscientist at the Allen Brain Institute, thinks thatmapping at the cellular scale will also redene anatomy. Traditionally, neuroanatomists have delineated brain regionspretty much by eye, identifying clusters of cells and patternsof connections that look the same.",
      "Sensory, motor, and cognitive functionsrely on the signaling dynamics of integrated circuitry that isestablished during brain development. The CNS develops in asequence of events characterized by an initial stage of neurogenesis and migration prenatally, followed by an extended lateprenatal and postnatal period of neuronal and glial differentiation, establishment of synaptic connections, and renement ofthe integrated circuits [Levitt, 2003]. In humans, neurogenesisstarts at 8 weeks of gestation and, in some areas of the brain, suchas the frontal lobe, maturation of CNS circuitry continues wellinto adolescence.",
      "To retaingenes that are more active when the brain is still undergoing corematurational processes in humans, we used BrainSpan to select autosomaltranscripts expressed at least 1.5-fold more during the early postnataldevelopment (018 months after birth) than in adulthood (2040 years ofage), with the nal networks consisting of 154 genes in the PFC (seeTable S4) and 72 genes in the NAcc (see Table S5).",
      "Because brain tissue from individuals in these cohorts is not accessible during their lives, many studies use postmortem tissue to identify molecules (e.g. , RNA, protein) that are associatedwith performance on cognitive tests prior to death. However, in these studies, brain regions used to examine the molecularmediators of resilience are typically selected based on already-known involvement in disease risk (e.g. , hippocampus andprefrontal cortex). It is possible that molecular changes that confer resilience originate in brain regions outside those classically affected in AD and are thus not typically selected for analyses.In addition, mechanisms and molecules important forresilience are likely expressed and act well before the time at which these tissues can be accessed. This lack of access tobrain tissue early in the disease course is a signicant barrier to understanding the molecules most closely associated withthe onset of resilience (and/or dementia). In addition, the ability to test mechanistic hypotheses is generally limited in humanpopulations, as the identication of molecules associated with cognitive outcomes is largely correlative [81]. Other potentialcaveats and considerations, such as the limitations associated with retrospective group assignments, have been highlighted elsewhere [81].",
      "It is a remarkablycomplex organ that integrates electrochemical signals, it receives and coordinatesactivities throughout the entire body. Despite the nonreplicative properties of thenervous system cells, it is proposed that through evolutionary pressures, thiscompartment has acquired distinct processes and mechanisms to minimizeneurodegeneration. One potential source of damage comes from our immunesystem, which has the capacity to scan the CNS and periphery for the presence offoreign antigens. The immune system is equipped with numerous effectorsmechanisms and can greatly alter the homeostasis and function of the CNS.",
      "In the brain, more than any other organ, function followsform, he says. Cellular resolution of expression patterns will provenecessary to uncover as yet unknown relationships betweencircuitry, cell type, and gene expression in the brain, saysArthur Toga, a neuroscientist at the University of California,Los Angeles, and Allen Brain Atlas advisor. Ed Lein, aneuroscientist at the Allen Brain Institute, thinks thatmapping at the cellular scale will also redene anatomy. Traditionally, neuroanatomists have delineated brain regionspretty much by eye, identifying clusters of cells and patternsof connections that look the same.",
      "The brain is the master organ of the body.It controls all other functions either directly or indirectly.The brain has two major types of cells, the neurons and glial cells.It is known that neurons, once differentiated are nondividing, and even in glial cells only a small fraction of them are dividing in adult and old ages (Korr, 1980).Thus it can be considered that most of the cells in an adult brain are postmitotic.Further, in the majority of the species the final number of differentiated neurons is reached very early in life (Dobbing, 1971) and therefore a neuron's life-span is almost equal to that of the whole animal.Considering the high metabolic activity in a neuronal cell, it must be of great necessity and importance to maintain the genomic integrity over a long period of time in order to keep up the fidelity of the cellular processes.Thus the processes of genomic damage and its repair assume special significance in nervous tissue.",
      "Because brain tissue from individuals in these cohorts is not accessible during their lives, many studies use postmortem tissue to identify molecules (e.g. , RNA, protein) that are associatedwith performance on cognitive tests prior to death. However, in these studies, brain regions used to examine the molecularmediators of resilience are typically selected based on already-known involvement in disease risk (e.g. , hippocampus andprefrontal cortex). It is possible that molecular changes that confer resilience originate in brain regions outside those classically affected in AD and are thus not typically selected for analyses.",
      "The brain is responsible for cognition, behavior, and much of what makes us uniquely human.The development of the brain is a highly complex process, and this process is reliant on precise regulation of molecular and cellular events grounded in the spatiotemporal regulation of the transcriptome.Disruption of this regulation can lead to neuropsychiatric disorders.RATIONALE: The regulatory, epigenomic, and transcriptomic features of the human brain have not been comprehensively compiled across time, regions, or cell types.Understanding the etiology of neuropsychiatric disorders requires sights into human development and disease.The brain is responsible for cognition, behavior, and much of what makes us uniquely human.The development of the brain is a highly complex process, and this process is reliant on precise regulation of molecular and cellular events grounded in the spatiotemporal regulation of the transcriptome.Disruption of this regulation can lead to neuropsychiatric disorders.RATIONALE: The regulatory, epigenomic, and transcriptomic features of the human brain have not been comprehensively compiled across time, regions, or cell types.Understanding the etiology of neuropsychiatric disorders requires sights into human development and disease.",
      "Nonetheless, several CNS measures,including behavioral phenotypes, correlated with both brainand blood 5-HT traits. One conspicuous correlation with 5-HTturnover was found for brain weight, hippocampal weightand hippocampal stem cell number. Studies that manipulate5-HT turnover independent of CNS 5-HT turnover are neededto determine whether these correlations reflect a result of 5HT homeostasis per se vs. a shared determinant that may inearly life impact the trajectory of brain development (Bonninet al. 2007; Janusonis et al. 2004; Mazer et al. 1997).",
      "In vitro,for example, blocking extrasynaptic NMDAtype glutamate receptors prevents amyloid-induced DSBs in neuronal cultures. In theaggregate, these data are all well controlledand very convincing. And yet, we find ourselves asking, How canthis possibly be? Do the neurons of our brainreally do serious damage to their genome everytime we execute a mental task? If 2 h of thinkingis enough to trigger DSBs in even a small percentage of our nerve cells, then each cell mustput its genome in jeopardy many times over thecourse of a year.",
      "Nonetheless, several CNS measures,including behavioral phenotypes, correlated with both brainand blood 5-HT traits. One conspicuous correlation with 5-HTturnover was found for brain weight, hippocampal weightand hippocampal stem cell number. Studies that manipulate5-HT turnover independent of CNS 5-HT turnover are neededto determine whether these correlations reflect a result of 5HT homeostasis per se vs. a shared determinant that may inearly life impact the trajectory of brain development (Bonninet al. 2007; Janusonis et al. 2004; Mazer et al. 1997).",
      "Although neuroimaging techniques unveil certain facets of CNSstructure and function, the human brains molecular profile is only attainable throughexamination of postmortem tissue. Many of the characteristics of the human brain may notbe conserved across species, emphasizing the inherent value of postmortem human tissue forinterrogating neuropsychiatric disorders (Hynd et al. 2003; Sutherland et al. 2016). Further,high-resolution maps for gene expression of the human brain across developmental periods,combined with separate genetic and proteomic datasets, can reveal potential neurobiologicalpathways and circuits underlying disease (Parikshak et al. 2013; Willsey et al. 2013). Addict Biol."
    ],
    [
      "Interestingly, fMRI studies in which personalized stressful imagery relating to pastexperiences was shown to healthy subjects, revealed significant increases in activationof the medial prefrontal cortex (mPFC), anterior cingulate, striatum, substantia nigra,thalamus, caudate, putamen, and hippocampus (Sinha, 2004), indicating a role for thestriatal-limbic-prefrontal circuits in response to emotional distress. In support of this,13eQTL mapping studies in the Miles laboratory implicate genes within the nucleusaccumbens (NAc) as potential modulators of anxiolytic-like phenotypes following acuteethanol administration (Putman, 2008; Wolen, 2012).",
      "Proc Natl Acad Sci USA103:780785123242LeDoux JE (2000) Emotion circuits in the brain. Annu RevNeurosci 23:155184Lee GP, Meador KJ, Loring DW, Allison JD, Brown WS, PaulLK, Pillai JJ, Lavin TB (2004) Neural substrates of emotionas revealed by functional magnetic resonance imaging. CogBehav Neurol 17:917Li CX, Wei X, Lu L, Peirce JL Williams RW, Waters RS (2005)Genetic analysis of barrel field size in the first somatosensory area (S1) in inbred and recombinant inbred strains ofmice.J Neurosci 21:35033514McGaugh JL (2004) The amygdala modulates the consolidationof memories of emotionally arousing experiences. AnnuRev Neurosci 27:128McIntyre CK, Power AE, Roozendaal B, McGaugh JL (2003)Role of the basolateral amygdala in memory consolidation. Ann NY Acad Sci 985:273293Meyer-Lindenberg A, Buckholtz JW, Kolachana B, Hariri AR,Pezawas L, Blasi G, Wabnitz A, Honea R, Verchinski B,Callicott JH, Egan M, Mattay V, Weinberger DR (2006)Neural mechanisms of genetic risk for impulsivity andviolence in humans.Somatosens Mol Res 22:141150Lin CH, Hansen S, Wang Z, Storm DR, Tapscott SJ, Olson JM(2005) The dosage of the neuroD2 transcription factorregulates amygdala development and emotional learning. Proc Natl Acad Sci USA 102:1487714882Ling EA, Paterson JA, Privat A, Mori S, Leblond CP (1973)Investigation of glial cells in semithin sections. I. Identification of glial cells in the brain of young rats. J CompNeurol 149:4371Lu L, Airey DC, Williams RW (2001) Complex trait analysis ofthe hippocampus: mapping and biometric analysis of twonovel gene loci with specific effects on hippocampal structure in mice.",
      "When attachments form in early infancy, activation and closer links are observed among neurobiological brain systems underpinning affiliation, reward, and stress management (Ulmer-Yaniv et al., 2016).Functional magnetic resonance imaging (fMRI) has been used to investigate the brain activity associated with humans' various social attachments (Feldman, 2017).These fMRIs provide evidence for three main inter-connected neural systems that integrate to establish, maintain, and enhance our attachments to others, including the rewardmotivation system (Berridge and Robinson, 1998), the embodied simulation/empathy network (Gallese, 2014), and mentalizing processes (Frith and Frith, 2006).The reward-motivation system comprises the striatum (nucleus accumbens, caudate, and putamen), amygdala, ventral tegmental area, orbitofrontal cortex, ventromedial prefrontal cortex, and anterior cingulate cortex (ACC).The existence of convergent projections from the cortex to the striatum, along with hippocampal and amygdala-striatal projections, places the striatum as a central entry port for processing emotional/motivational information supporting human attachment (Haber and Knutson, 2010;Robinson et al., 2012;Pauli et al., 2016).The reward-motivation system employs DA and oxytocin rich pathways (Schultz, 2000;Berridge et al., 2009;Haber and Knutson, 2010) and supports multiple attachment-related motivational behaviors, such as social orienting, social seeking, and maintaining contact (Acevedo et al., 2012;Chevallier et al., 2012).Attachments have an intrinsic motivational value that combine immediate hedonic responses with approach motivation, goal-directed behavior, and learning (Berridge and Robinson, 1998).",
      "Genetics of emotional regulation: therole of the serotonin transporter in neural function. Trends CognSci 10: 182191. Hefner K, Holmes A (2007). Ontogeny of fear-, anxiety- anddepression-related behavior across adolescence in C57BL/6Jmice. Behav Brain Res 176: 210215. Herman JP, Ostrander MM, Mueller NK, Figueiredo H (2005). Limbic system mechanisms of stress regulation: hypothalamopituitaryadrenocortical axis. Prog Neuropsychopharmacol BiolPsychiatry 29: 12011213. Herry C, Bach DR, Esposito F, Di Salle F, Perrig WJ, Scheffler Ket al (2007). Processing of temporal unpredictability in humanand animal amygdala. J Neurosci 27: 59585966.Nat Neurosci 8: 828834. Phelps EA, LeDoux JE (2005). Contributions of the amygdala toemotion processing: from animal models to human behavior. Neuron 48: 175187. Porsolt RD, Bertin A, Jalfre M (1978). Behavioural despair in ratsand mice: strain differences and the effects of imipramine. Eur JPharmacol 51: 291294. Quirk GJ, Mueller D (2007). Neural mechanisms of extinctionlearning and retrieval. Neuropsychopharmacology 33: 5672. Radley JJ, Rocher AB, Miller M, Janssen WG, Liston C, Hof PR et al(2006). Repeated stress induces dendritic spine loss in the ratmedial prefrontal cortex. Cereb Cortex 16: 313320.",
      "Like most, if not all, neural phenotypes, stress,anxiety, and other emotion-related traits are extremely complex and are defined by theinterplay of multiple genetic, environmental, experiential, and epigenetic factors. The work presented in this dissertation is a multi-scalar, integrative analysis of themolecular and neuroanatomic substrates that underlie emotion-related behavior. Theamygdala is a principle component of the limbic system that controls emotionality. UsingBXD recombinant inbred (RI) mice as model organisms, the anatomy and cellulararchitecture of the amygdalaspecifically, the basolateral amygdala (BLA)wasexamined to assess the level of structural variation in this brain region.To this end, weemployed a repeated restraint stress protocol that has been shown to cause significantalterations in the morphology of principal neurons in three key corticolimbic regionsknown to mediate the effects of stress: medial prefrontal cortex (mPFC), amygdala andhippocampus (e.g. , Vyas et al. , 2002; Vyas et al. , 2003; Govindarajan et al. , 2006;Bennur et al. , 2007; Shansky et al. , 2009).Sensory inputs with emotional components aretransmitted to the amygdala where they are processed and further relayed to other regionsto modulate autonomic and behavioral responses, and to form emotional memories(LeDoux, 2000; Rosen, 2004). As a neural substrate of emotionality, manyneuropsychiatric disorders have been associated with structural changes in the amygdala. Individuals with genetically predisposed susceptibility to anxiety and depression havebeen shown to have higher amygdala reactivity and smaller amygdala volumes (Pezawaset al. , 2005). Structural changes in the amygdala have also been associated with traumaticstress disorder, bipolar disorder, and aggressive behavior (Hayek et al.These studies have uncovered complex geneticsunderlying behavior with multiple loci modulating stress responsiveness, fear, andanxiety levels in mice (Willis-Owen & Flint, 2006). Significant concordance betweenhuman and mouse traits also exists, e.g. , the gene Rgs2 was shown to modulate anxiety inmice, and was subsequently found to be associated with anxiety in human (Yalcin et al. ,2004; Smoller et al. , 2008). 1.3Neuroanatomy of Stress and Emotion-Related BehaviorThe amygdala is a neural structure central to the experience of emotions andexpression of emotional behavior.",
      "Alterations in BDNF expression werealso found in response to emotions such asanxiety or fear in rodents (Rasmusson et al. ,2002), and it has been shown that BDNF affects emotional preferences in humans (Gasicet al. , 2009). It remains to be determined howthe stress itself or the associated behavioral responses contribute to mediating these changes. From this perspective, sh, whose brain organization is very similar to that of higher vertebrates, but is generally considered free ofemotional reactions, is interesting as an animalmodel of stress.",
      "enhance our attachments to others, including the rewardmotivation system (Berridge and Robinson, 1998), the embodiedsimulation/empathy network (Gallese, 2014), and mentalizingprocesses (Frith and Frith, 2006). The reward-motivationsystem comprises the striatum (nucleus accumbens, caudate,and putamen), amygdala, ventral tegmental area, orbitofrontalcortex, ventromedial prefrontal cortex, and anterior cingulatecortex (ACC). The existence of convergent projections fromthe cortex to the striatum, along with hippocampal andamygdala-striatal projections, places the striatum as a centralentry port for processing emotional/motivational informationsupporting human attachment (Haber and Knutson, 2010;Robinson et al. , 2012; Pauli et al. , 2016).We focused on theprefrontal cortex due to its association with cognitive, emotionalfunctions, impulse control, and adaptive behaviors (Morecraftand Yeterian, 2002; Bechara and Van Der Linden, 2005), andthe striatum for its involvement in the reward motivation systemand potential to relate to attachment formation in infancyspecifically (Feldman, 2017). Convergent projections from thecortex to the striatum, along with hippocampal and amygdalastriatal projections, places the striatum as a central entry portfor processing emotional/motivational information supportinghuman attachments (Haber and Knutson, 2010; Robinson et al. ,2012; Pauli et al. , 2016; Feldman, 2017).",
      "Central nervous system regions that regulate mood,emotion, feeding and reward are prominent sites of 5-HTsynthesis and release (Steinbusch 1981). As such, a numberof disorders have been reported to display alterations in CNS5-HT homeostasis, including anxiety, depression, obsessivecompulsive disorder and addiction (Barondes 1994). Althougha subject of significant debate (Risch et al. 2009), biochemicaland genetic evidence continues to drive consideration thatrisk for depression in some individuals may be linked to alimited capacity for normal brain 5-HT signaling.",
      "enhance our attachments to others, including the rewardmotivation system (Berridge and Robinson, 1998), the embodiedsimulation/empathy network (Gallese, 2014), and mentalizingprocesses (Frith and Frith, 2006). The reward-motivationsystem comprises the striatum (nucleus accumbens, caudate,and putamen), amygdala, ventral tegmental area, orbitofrontalcortex, ventromedial prefrontal cortex, and anterior cingulatecortex (ACC). The existence of convergent projections fromthe cortex to the striatum, along with hippocampal andamygdala-striatal projections, places the striatum as a centralentry port for processing emotional/motivational informationsupporting human attachment (Haber and Knutson, 2010;Robinson et al. , 2012; Pauli et al. , 2016).We focused on theprefrontal cortex due to its association with cognitive, emotionalfunctions, impulse control, and adaptive behaviors (Morecraftand Yeterian, 2002; Bechara and Van Der Linden, 2005), andthe striatum for its involvement in the reward motivation systemand potential to relate to attachment formation in infancyspecifically (Feldman, 2017). Convergent projections from thecortex to the striatum, along with hippocampal and amygdalastriatal projections, places the striatum as a central entry portfor processing emotional/motivational information supportinghuman attachments (Haber and Knutson, 2010; Robinson et al. ,2012; Pauli et al. , 2016; Feldman, 2017).",
      "(2010)Genetic control over the resting brain. Proc Natl Acad Sci U S A 107, 12231228. Glasser, M.F. , Smith, S.M. , Marcus, D.S. , Andersson, J.L.R. , Auerbach, E.J. , Behrens, T.E.J. ,Coalson, T.S. , Harms, M.P. , Jenkinson, M., Moeller, S., Robinson, E.C. , Sotiropoulos, S.N. ,Xu, J., Yacoub, E., Ugurbil, K. & Van Essen, D.C. (2016) The Human Connectome Projectsneuroimaging approach. Nat Neurosci 19, 11751187. Gracia-Rubio, I., Moscoso-Castro, M., Pozo, O.J. , Marcos, J., Nadal, R. & Valverde, O. (2016)Maternal separation induces neuroinflammation and long-lasting emotional alterations inmice.",
      "He and othersconsidered that hormones released by stressful experiences couldenhance memory consolidation, indicating particularly the hormonesepinephrine and glucocorticoids as memory modulators (McGaugh &Roozendaal, 2009). It was suggested that several brain regions work insynergy to assure that emotionally significant experiences are wellremembered, and this could prepare the organism for future experiences by inducing long-term behavioral changes (Bahtiyar, Karaca,Henckens, & Roozendaal, 2020; McGaugh, 2013).",
      "Central nervous system regions that regulate mood,emotion, feeding and reward are prominent sites of 5-HTsynthesis and release (Steinbusch 1981). As such, a numberof disorders have been reported to display alterations in CNS5-HT homeostasis, including anxiety, depression, obsessivecompulsive disorder and addiction (Barondes 1994). Althougha subject of significant debate (Risch et al. 2009), biochemicaland genetic evidence continues to drive consideration thatrisk for depression in some individuals may be linked to alimited capacity for normal brain 5-HT signaling."
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