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Nature Reviews. Neuroscience Jun 2021Childhood socio-economic status (SES), a measure of the availability of material and social resources, is one of the strongest predictors of lifelong well-being. Here we... (Review)
Review
Childhood socio-economic status (SES), a measure of the availability of material and social resources, is one of the strongest predictors of lifelong well-being. Here we review evidence that experiences associated with childhood SES affect not only the outcome but also the pace of brain development. We argue that higher childhood SES is associated with protracted structural brain development and a prolonged trajectory of functional network segregation, ultimately leading to more efficient cortical networks in adulthood. We hypothesize that greater exposure to chronic stress accelerates brain maturation, whereas greater access to novel positive experiences decelerates maturation. We discuss the impact of variation in the pace of brain development on plasticity and learning. We provide a generative theoretical framework to catalyse future basic science and translational research on environmental influences on brain development.
Topics: Adolescent; Adult Survivors of Child Adverse Events; Adverse Childhood Experiences; Animals; Bibliometrics; Brain; Cerebral Cortex; Child; Child, Preschool; Cross-Sectional Studies; Environment; Female; Humans; Infant; Learning; Longitudinal Studies; Male; Minority Groups; Nerve Net; Neuronal Plasticity; Neurosciences; Organ Size; Pregnancy; Social Class; Stress, Physiological
PubMed: 33911229
DOI: 10.1038/s41583-021-00457-5 -
Pediatric Research Dec 2017BackgroundIn this study, we examined the hypothesis that weight gain and linear growth during the first years of life influence the onset of puberty both in girls and in...
BackgroundIn this study, we examined the hypothesis that weight gain and linear growth during the first years of life influence the onset of puberty both in girls and in boys.MethodsA cohort of 157 healthy children, aged 6-9 years, was evaluated and their growth patterns were analyzed retrospectively. Repeated measures mixed model was used to examine the longitudinal anthropometric data.ResultsGirls with pubertal signs were heavier than their peers starting at 9 months of age (P=0.02), and the difference became more evident over time (P<0.001). Accelerated weight gain between 6 and 15 months of age was found to increase the odds of having a pubertal sign at the study visit (odds ratio (OR)=34.5) after adjusting for birth weight, gestational age and current age, height, weight, and BMI (P=0.004). Anthropometric indices of boys with or without pubertal signs were not significantly different at the study visit, but boys with accelerated height gain between 9 and 15 months of age were more likely to have pubertal signs (OR=15.8) after adjusting for birth weight, gestational age and current age, height, weight, and BMI (P=0.016).ConclusionEarly growth acceleration might be important for the timing of puberty in both genders.
Topics: Child; Female; Growth; Humans; Infant; Longitudinal Studies; Male; Puberty; Retrospective Studies
PubMed: 28902184
DOI: 10.1038/pr.2017.194 -
American Journal of Human Biology : the... Jun 2022Childhood obesity is a systemic disease with multiple downstream consequences, including shifts in timing of growth and development. It has been documented that children...
OBJECTIVES
Childhood obesity is a systemic disease with multiple downstream consequences, including shifts in timing of growth and development. It has been documented that children with high body mass index (BMI) show accelerated timing of dental development, but the mechanism for this acceleration is unknown. Prior work has suggested that inflammation and/or nutrition may play a role. We investigate the potential association between diet (caloric intake, macronutrients), obesity, and accelerated dental development.
METHODS
Children and adolescents (age 10-15; n = 112) were recruited from dental clinics at the University of Illinois Chicago. We collected subjects' height, weight, panoramic radiographic records, and each subject filled out a Block Food Frequency Questionnaire.
RESULTS
The only macronutrient level associated with BMI was a negative correlation to Total Fat consumption (p = .01), though this relationship was not significant in the path analysis (p > .05). Regression analyses indicated that BMI (p = .003) and total caloric intake (controlling for BMI; rho = 0.19; p = .04) were both significantly correlated with timing of dental development. However, when a path analysis was conducted, it was revealed that only BMI was statistically significant (p = .008).
CONCLUSIONS
Body mass index percentile, regardless of caloric intake, is positively associated with accelerated dental development. While it is possible that excess caloric intake itself plays a minor role in timing of dental development, we do not see unambiguous evidence for this in our sample. We posit that another mechanism, such as inflammation, may be the link between obesity status and dental development.
Topics: Adolescent; Body Mass Index; Body Weight; Chicago; Child; Cross-Sectional Studies; Energy Intake; Humans; Inflammation; Pediatric Obesity
PubMed: 35064944
DOI: 10.1002/ajhb.23721 -
Pediatric Pulmonology Feb 2018Fetal growth and rapid postnatal weight gain are associated with adverse respiratory outcomes in childhood. However, the preterm-born population is less well studied. We...
OBJECTIVES
Fetal growth and rapid postnatal weight gain are associated with adverse respiratory outcomes in childhood. However, the preterm-born population is less well studied. We assessed if the increased respiratory symptoms associated with altered fetal growth and infant weight gain were mediated by early factors.
STUDY DESIGN
We used data from our cohort of preterm- and term-born (n = 4284 and 2865) children, aged 1-10 years. Respiratory outcomes obtained from a respiratory questionnaire were regressed on measures of fetal growth and infant weight gain, defined as >0.67 SD change in fetal measurement or weight between birth and nine months of age, then adjusted for covariates. We used mediation analysis to investigate which variables were effect modifiers.
RESULTS
Accelerated fetal growth between the 1st trimester and birth (OR 2.01; 95%CI 1.25, 2.32), and between the 2nd trimester and birth (1.60; 1.15, 2.22) was associated with increased wheeze-ever in preterm-born children. Rapid infant weight gain was associated with increased wheeze-ever (1.22; 1.02, 1.45); children born ≤32 weeks' gestation exhibiting rapid weight gain had fivefold higher risk of wheeze-ever compared to term-born without weight gain. Current maternal smoking and gestational age were identified as candidate mediating effects.
CONCLUSIONS
Our study suggested that antenatal and postnatal growth rates are important for future respiratory health in preterm-born children, and that their effects may be mediated by modifiable factors. Minimizing exposure to environmental pollutants, especially maternal tobacco smoking, may improve outcomes.
Topics: Child; Child, Preschool; Female; Fetal Development; Gestational Age; Humans; Infant; Infant, Newborn; Infant, Premature; Male; Pregnancy; Pregnancy Trimester, First; Pregnancy Trimester, Second; Respiration Disorders; Respiratory Sounds; Retrospective Studies; Risk Factors; Surveys and Questionnaires; Term Birth; Weight Gain
PubMed: 29168321
DOI: 10.1002/ppul.23920 -
PLoS Genetics May 2021The plastochron, the time interval between the formation of two successive leaves, is an important determinant of plant architecture. We genetically and phenotypically...
The plastochron, the time interval between the formation of two successive leaves, is an important determinant of plant architecture. We genetically and phenotypically investigated many-noded dwarf (mnd) mutants in barley. The mnd mutants exhibited a shortened plastochron and a decreased leaf blade length, and resembled previously reported plastochron1 (pla1), pla2, and pla3 mutants in rice. In addition, the maturation of mnd leaves was accelerated, similar to pla mutants in rice. Several barley mnd alleles were derived from three genes-MND1, MND4, and MND8. Although MND4 coincided with a cytochrome P450 family gene that is a homolog of rice PLA1, we clarified that MND1 and MND8 encode an N-acetyltransferase-like protein and a MATE transporter-family protein, which are respectively orthologs of rice GW6a and maize BIGE1 and unrelated to PLA2 or PLA3. Expression analyses of the three MND genes revealed that MND1 and MND4 were expressed in limited regions of the shoot apical meristem and leaf primordia, but MND8 did not exhibit a specific expression pattern around the shoot apex. In addition, the expression levels of the three genes were interdependent among the various mutant backgrounds. Genetic analyses using the double mutants mnd4mnd8 and mnd1mnd8 indicated that MND1 and MND4 regulate the plastochron independently of MND8, suggesting that the plastochron in barley is controlled by multiple genetic pathways involving MND1, MND4, and MND8. Correlation analysis between leaf number and leaf blade length indicated that both traits exhibited a strong negative association among different genetic backgrounds but not in the same genetic background. We propose that MND genes function in the regulation of the plastochron and leaf growth and revealed conserved and diverse aspects of plastochron regulation via comparative analysis of barley and rice.
Topics: Alleles; CRISPR-Cas Systems; Cell Division; Gene Expression Regulation, Plant; Genes, Plant; Hordeum; Mutation; Oryza; Phenotype; Plant Cells; Plant Leaves; Time Factors
PubMed: 33970916
DOI: 10.1371/journal.pgen.1009292 -
American Journal of Physiology.... Apr 2020Liver resection induces robust liver regrowth or regeneration to compensate for the lost tissue mass. In a clinical setting, pregnant women may need liver resection...
Liver resection induces robust liver regrowth or regeneration to compensate for the lost tissue mass. In a clinical setting, pregnant women may need liver resection without terminating pregnancy in some cases. However, how pregnancy affects maternal liver regeneration remains elusive. We performed 70% partial hepatectomy (PH) in nonpregnant mice and gestation mice, and histologically and molecularly compared their liver regrowth during the next 4 days. We found that compared with the nonpregnant state, pregnancy altered the molecular programs driving hepatocyte replication, indicated by enhanced activities of epidermal growth factor receptor and STAT5A, reduced activities of cMet and p70S6K, decreased production of IL-6, TNFα, and hepatocyte growth factor, suppressed cyclin D1 expression, increased cyclin A1 expression, and early activated cyclin A2 expression. As a result, pregnancy allowed the remnant hepatocytes to enter the cell cycle at least 12 h earlier, increased hepatic fat accumulation, and enhanced hepatocyte mitosis. Consequently, pregnancy ameliorated maternal liver regeneration following PH. In addition, a report showed that maternal liver regrowth after PH is driven mainly by hepatocyte hypertrophy rather than hyperplasia during the second half of gestation in young adult mice. In contrast, we demonstrate that maternal liver relies mainly on hepatocyte hyperplasia instead of hypertrophy to restore the lost mass after PH. Overall, we demonstrate that pregnancy facilitates maternal liver regeneration likely via triggering an early onset of hepatocyte replication, accumulating excessive liver fat, and promoting hepatocyte mitosis. The results from our current studies enable us to gain more insights into how maternal liver regeneration progresses during gestation. We demonstrate that pregnancy may generate positive effects on maternal liver regeneration following partial hepatectomy, which are manifested by early entry of the cell cycle of remnant hepatocytes, increased hepatic fat accumulation, enhanced hepatocyte mitosis, and overall accelerated liver regrowth.
Topics: Animals; Body Weight; Female; Hepatectomy; Liver; Liver Regeneration; Mice; Mice, Inbred C57BL; Mitosis; Organ Size; Pregnancy
PubMed: 32003603
DOI: 10.1152/ajpgi.00125.2019 -
American Journal of Obstetrics and... Sep 2016Surgery is currently the mainstay treatment for solid tumors and many benign diseases, including endometriosis, and women tend to receive substantially more surgeries...
BACKGROUND
Surgery is currently the mainstay treatment for solid tumors and many benign diseases, including endometriosis, and women tend to receive substantially more surgeries than men mainly because of gynecological and cosmetic surgeries. Despite its cosmetic, therapeutic, or even life-saving benefits, surgery is reported to increase the cancer risk and promotes cancer metastasis. Surgery activates adrenergic signaling, which in turn suppresses cell-mediated immunity and promotes angiogenesis and metastasis. Because immunity, angiogenesis, and invasiveness are all involved in the pathophysiology of endometriosis, it is unclear whether surgery may accelerate the development of endometriosis.
OBJECTIVE
The objective of the study was to test the hypothesis that surgery activates adrenergic signaling, increases angiogenesis, and accelerates the growth of endometriotic lesions.
STUDY DESIGN
This was a prospective, randomized experimentation. The first experiment used 42 female adult Balb/C mice, and the second used 90 female adult Balb/C mice. In experiment 1, 3 days after the induction of endometriosis, mice were randomly divided into 3 groups of approximately equal sizes, control, laparotomy, and mastectomy. In experiment 2, propranolol infusion via Alzet pumps was used to forestall the effect of sympathetic nervous system activation by surgery. In both experiments, mice were evaluated 2 weeks after surgery. Lesion size, hotplate latency, and immunohistochemistry analysis of vascular endothelial growth factor, CD31-positive microvessels, proliferating cell nuclear antigen, phosphorylated cyclic adenosine monophosphate-responsive element-binding protein, β2-adrenergic receptor (ADRB)-2, ADRB1, ADRB3, ADRA1, and ADRA2 in ectopic implants.
RESULTS
Both mastectomy and laparotomy increased lesion weight and exacerbated hyperalgesia, increased microvessel density and elevated the immunoreactivity against ADRB2, phosphorylated cyclic adenosine monophosphate-responsive element-binding protein, vascular endothelial growth factor, and proliferating cell nuclear antigen but not ADRB1, ADRB3, ADRA1, and ADRA2, suggesting activated adrenergic signaling, increased angiogenesis, and accelerated growth of endometriotic lesions. β-Blockade completely abrogated the facilitory effect of surgery, further underscoring the critical role of β-adrenergic signaling in mediating the effect of surgery.
CONCLUSION
Surgery activates adrenergic signaling, increases angiogenesis, and accelerates the growth of endometriotic lesions in the mouse, but such a facilitory effect of surgery can be completely abrogated by β-blockade. Whether surgery can promote the development of endometriosis in humans warrants further investigation.
Topics: Animals; CREB-Binding Protein; Cell Proliferation; Disease Models, Animal; Endometriosis; Female; Laparotomy; Mice; Mice, Inbred BALB C; Microvessels; Neovascularization, Pathologic; Proliferating Cell Nuclear Antigen; Receptors, Adrenergic, beta; Signal Transduction; Vascular Endothelial Growth Factor A
PubMed: 26945602
DOI: 10.1016/j.ajog.2016.02.055 -
PloS One 2020The purpose of this systematic review and meta-analysis of the literature was to analyze and evaluate the impact of prematurity and accelerated weight gain on the risk... (Meta-Analysis)
Meta-Analysis
The purpose of this systematic review and meta-analysis of the literature was to analyze and evaluate the impact of prematurity and accelerated weight gain on the risk of childhood and adolescent obesity. CINAHL, Embase, PubMed, and Web of Science databases were searched until December 2019 which yielded 19 studies with a total of 169,439 children enrolled were systematically reviewed. The results revealed that preterm infants had a greater likelihood of childhood obesity (defined as BMI ≥95th percentile for age-sex), than term infants (OR = 1.19, 95% CI [1.13, 1.26]). However, no difference of childhood obesity was found between "small for gestational age"(SGA) and "appropriate for gestational age"(AGA) among preterms. Accelerated weight gain (defined as weight gain velocity during first two years after birth) significantly increased the likelihood of subsequent childhood obesity among preterms (aOR = 1.87, 95% CI [1.57, 2.231]). In conclusion, accelerated weight gain at infancy among preterm children may be a critical contributor to obesity in later life. Establishing optimal growth trajectories and timely referral to health care providers may be of clinical importance.
Topics: Humans; Infant, Premature; Pediatric Obesity; Risk; Weight Gain
PubMed: 32369502
DOI: 10.1371/journal.pone.0232238 -
Acta Bio-medica : Atenei Parmensis Jan 2022Early puberty (EP) in girls is defined as the onset of thelarche that begins after 6 years and before 8 years and/or acceleration in the tempo of pubertal development....
INTRODUCTION
Early puberty (EP) in girls is defined as the onset of thelarche that begins after 6 years and before 8 years and/or acceleration in the tempo of pubertal development. The stage of puberty and the ovarian volume at presentation and the effect of treatment with GnRH analogue (GnRHa) on final adult height are still debated.
PATIENTS AND METHODS
We analyzed the data of 22 girls, who presented early and fast puberty (FEP). The clinical stage of puberty, hormonal levels and the ovarian volume (OV) (measured by ovarian ultra-sonography) at presentation were studied. We recorded the effects of 3 years treatment with GnRHa on their growth in relation to their mid parental height, pubertal progression, and bone maturation.
RESULTS AND CONCLUSION
GnRHa therapy decreased the fast progress of puberty, skeletal maturation, and GV/year. It was successful in increasing the predicted final adult height comparable to or surpassing their mid-parenteral height. A larger OV at presentation was associated with reduced Ht-SDS after 3 years of GnRHa treatment. Clearly, a definitive evaluation of the efficacy of GnRHa as treatment for EFP in girls will require expanded and concerted studies.
Topics: Body Height; Bone Development; Female; Gonadotropin-Releasing Hormone; Humans; Puberty; Puberty, Precocious
PubMed: 35075088
DOI: 10.23750/abm.v92i6.10809 -
Plant Physiology Dec 2015Growth of tissues is highly reproducible; yet, growth of individual cells in a tissue is highly variable, and neighboring cells can grow at different rates. We analyzed...
Growth of tissues is highly reproducible; yet, growth of individual cells in a tissue is highly variable, and neighboring cells can grow at different rates. We analyzed the growth of epidermal cell lineages in the Arabidopsis (Arabidopsis thaliana) sepal to determine how the growth curves of individual cell lineages relate to one another in a developing tissue. To identify underlying growth trends, we developed a continuous displacement field to predict spatially averaged growth rates. We showed that this displacement field accurately describes the growth of sepal cell lineages and reveals underlying trends within the variability of in vivo cellular growth. We found that the tissue, individual cell lineages, and cell walls all exhibit growth rates that are initially low, accelerate to a maximum, and decrease again. Accordingly, these growth curves can be represented by sigmoid functions. We examined the relationships among the cell lineage growth curves and surprisingly found that all lineages reach the same maximum growth rate relative to their size. However, the cell lineages are not synchronized; each cell lineage reaches this same maximum relative growth rate but at different times. The heterogeneity in observed growth results from shifting the same underlying sigmoid curve in time and scaling by size. Thus, despite the variability in growth observed in our study and others, individual cell lineages in the developing sepal follow similarly shaped growth curves.
Topics: Arabidopsis; Cell Division; Cell Lineage; Cell Wall; Flowers; Models, Biological; Plant Epidermis
PubMed: 26432876
DOI: 10.1104/pp.15.00839