Independent Behavior of the Human Infant

2018 ◽  
pp. 178-204 ◽  
Author(s):  
HARRIET L. RHEINGOLD
Keyword(s):  
Human Infant ◽  
Independent Behavior

REGIONAL BETA-ENDORPHIN LEVELS MAPPED IN THE HYPOTHALAMUS OF THE HUMAN INFANT

Analgesia ◽  
1995 ◽  
Vol 1 (4) ◽  
pp. 627-634
Author(s):  
A. Pasi ◽  
B. Qu ◽  
C. Bernasconi ◽  
H. Mahler ◽  
W. Bär
Keyword(s):  
Human Infant ◽  
Beta Endorphin

scholarly journals Infant gut microbiome composition is associated with non-social fear behavior in a pilot study

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Alexander L. Carlson ◽  
Kai Xia ◽  
M. Andrea Azcarate-Peril ◽  
Samuel P. Rosin ◽  
Jason P. Fine ◽  
...  
Keyword(s):  
Pilot Study ◽  
Gut Microbiome ◽  
Brain Structures ◽  
Experimental Manipulation ◽  
Human Infant ◽  
Microbiome Composition ◽  
Social Fear ◽  
Infant Gut Microbiome ◽  
First Year Of Life ◽  
Fear Behavior

AbstractExperimental manipulation of gut microbes in animal models alters fear behavior and relevant neurocircuitry. In humans, the first year of life is a key period for brain development, the emergence of fearfulness, and the establishment of the gut microbiome. Variation in the infant gut microbiome has previously been linked to cognitive development, but its relationship with fear behavior and neurocircuitry is unknown. In this pilot study of 34 infants, we find that 1-year gut microbiome composition (Weighted Unifrac; lower abundance of Bacteroides, increased abundance of Veillonella, Dialister, and Clostridiales) is significantly associated with increased fear behavior during a non-social fear paradigm. Infants with increased richness and reduced evenness of the 1-month microbiome also display increased non-social fear. This study indicates associations of the human infant gut microbiome with fear behavior and possible relationships with fear-related brain structures on the basis of a small cohort. As such, it represents an important step in understanding the role of the gut microbiome in the development of human fear behaviors, but requires further validation with a larger number of participants.

scholarly journals 146 Prematurity Blunts the Protein Synthetic Response of Skeletal Muscle to Insulin and Amino Acids

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 118-119
Author(s):  
Teresa A Davis ◽  
Marko Rudar ◽  
Jane Naberhuis ◽  
Agus Suryawan ◽  
Marta Fiorotto
Keyword(s):  
Skeletal Muscle ◽  
Amino Acids ◽  
Protein Synthesis ◽  
Amino Acid ◽  
Body Weight Gain ◽  
Human Infant ◽  
Long Term Effects ◽  
Plasma Insulin Concentration ◽  
Akt Phosphorylation ◽  
Relative Body Weight

Abstract Livestock animals are important dual-purpose models that benefit both agricultural and biomedical research. The neonatal pig is an appropriate model for the human infant to assess long-term effects of early life nutrition on growth and metabolic outcomes. Previously we have demonstrated that prematurity blunts the feeding-induced stimulation of translation initiation and protein synthesis in skeletal muscle of neonatal pigs. The objective of this study was to determine whether reduced sensitivity to insulin and/or amino acids drives this blunted response. Pigs were delivered by caesarean section at preterm (PT, 103 d gestation) or at term (T, 112 d gestation) and fed parenterally for 4 d. On day 4, pigs were subject to euinsulinemic-euaminoacidemic-euglycemic (FAST), hyperinsulinemic-euaminoacidemic-euglycemic (INS), or euinsulinemic-hyperaminoacidemic-euglycemic (AA) clamps for 120 min, yielding six treatments: PT-FAST (n = 7), PT-INS (n = 9), PT-AA (n = 9), T-FAST (n = 8), T-INS (n = 9), and T-AA (n = 9). A flooding dose of L-[4-3H]Phe was injected into pigs 30 min before euthanasia. Birth weight and relative body weight gain were lower in PT than T pigs (P < 0.001). Plasma insulin concentration was increased from ~3 to ~100 µU/mL in INS compared to FAST and AA pigs (P < 0.001); plasma BCAA concentration was increased from ~250 to ~1,000 µmol/L in AA compared to FAST and INS pigs (P < 0.001). Despite achieving similar insulin and amino acid levels, longissimus dorsi AKT phosphorylation, mechanistic target of rapamycin (mTOR)·Rheb abundance, mTOR activation, and protein synthesis were lower in PT-INS than T-INS pigs (Table 1). Although amino-acid induced dissociation of Sestrin2 from GATOR2 was not affected by prematurity, mTOR·RagA abundance, mTOR·RagC abundance, mTOR activation, and protein synthesis were lower in PT-AA than T-AA pigs. The impaired capacity of premature skeletal muscle to respond to insulin or amino acids and promote protein synthesis likely contributes to reduced lean mass accretion. Research was supported by NIH and USDA.

scholarly journals Effect of Dietary Fat Composition and 2’Fucosyllactose on Neonatal Piglet Growth and Organ Lipid Composition

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1038-1038
Author(s):  
Michael Miklus ◽  
Pedro Prieto ◽  
Cynthia Barber ◽  
Robert Rhoads ◽  
Samer El-Kadi
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Fatty Acid ◽  
Body Weight Gain ◽  
Dietary Fatty Acids ◽  
The Body ◽  
The Other ◽  
Human Infant ◽  
Lps Challenge ◽  
Group 3

Abstract Objectives The objectives of this study were to determine the effect of 2’fucosyllactose (2’FL) and fat blends on growth, body composition and fatty acid profile of the liver and brain using the neonatal pig as a model for the human infant. Methods Pigs (3 d old) were randomly assigned to either: 1. control, 2. Palm Olein (PO) fat blend – Low 2'-FL, 3. PO – High 2'-FL, 4. High oleic acid (HO) – Low 2'-FL, 5. HO FB – High 2'-FL, 6. PO FB – GLA, or 7. kept with their sows. Pigs in groups 1 to 6 received 250 ml·kg−1·d−1 of formula in 5 equal meals for 15 d. On day 14 of the study, groups 1–6 received intraperitoneal E. coli LPS challenge at 100 µg·kg−1 weight. Results Body weight was greater for piglets fed by sows than those in the other groups (P < 0.001). In addition, % fat and bone mineral content were higher in the sow-fed group while lean % was less sow-fed piglets (group 7) compared with those in the other groups (P < 0.05). Only longissimus weight expressed as a % of body weight, was greater for group 7 compared with all other groups (P < 0.001). Soleus, semitendinosus, brain, heart and spleen weights as a % of body weight were similar across all groups. However, liver weight as a % of body weight was greater in groups 1–6 (3.7%) compared with group 7 (2.8%; P < 0.001). The proportion of brain 16:1 fatty acid was less (0.83%) for groups 1–6 than for group 7 pigs (1.08%; P < 0.0001). The proportion of 20:3 N6 was greatest (0.66%) for group 3 compared with groups 1 and 4 (0.55%; P < 0.05). In addition, the proportion of 20:5 N3 was greatest (0.12%) for group 3 compared with groups 1 and 7 (0.07%; P < 0.05). The proportion of liver 16:1, 18:0, and 18:1 cis-11 fatty acids were greater for group 7 (2.3, 23, 2.2%) than groups 1–6 (0.2, 20, 1.2%; P < 0.0001). Conversely, the contribution of 14:0, 18:1 cis-9, 18:3 N6 cis-6,9,12, and 22:6 N3 were greater for pigs in groups 1–6 (1.3, 0.6, and 14, 7.8%) compared with those in group 7 (0.5, 8.5, 0.2 and 3.5%; P < 0.0001). Conclusions Our data suggest that feeding 2’fucosyllactose had no effect on the body weight gain and composition in neonatal pigs. Our data also suggest that dietary fatty acids have a greater effect on liver than on brain fatty acid composition. Funding Sources Funding for the work was provided by Perrigo Nutritionals, LLC.

scholarly journals The efficiency of murine MLL-ENL–driven leukemia initiation changes with age and peaks during neonatal development

2019 ◽  
Vol 3 (15) ◽  
pp. 2388-2399 ◽  
Author(s):  
Theresa Okeyo-Owuor ◽  
Yanan Li ◽  
Riddhi M. Patel ◽  
Wei Yang ◽  
Emily B. Casey ◽  
...  
Keyword(s):  
Myeloid Leukemia ◽  
Transgene Expression ◽  
Target Genes ◽  
Lymphoblastic Leukemia ◽  
Human Infant ◽  
Driver Mutations ◽  
Hematopoietic Progenitors ◽  
Adult Mice ◽  
Almost All ◽  
Infant Leukemia

Abstract MLL rearrangements are translocation mutations that cause both acute lymphoblastic leukemia and acute myeloid leukemia (AML). These translocations can occur as sole clonal driver mutations in infant leukemias, suggesting that fetal or neonatal hematopoietic progenitors may be exquisitely sensitive to transformation by MLL fusion proteins. To test this possibility, we used transgenic mice to induce one translocation product, MLL-ENL, during fetal, neonatal, juvenile and adult stages of life. When MLL-ENL was induced in fetal or neonatal mice, almost all died of AML. In contrast, when MLL-ENL was induced in adult mice, most survived for >1 year despite sustained transgene expression. AML initiation was most efficient when MLL-ENL was induced in neonates, and even transient suppression of MLL-ENL in neonates could prevent AML in most mice. MLL-ENL target genes were induced more efficiently in neonatal progenitors than in adult progenitors, consistent with the distinct AML initiation efficiencies. Interestingly, transplantation stress mitigated the developmental barrier to leukemogenesis. Since fetal/neonatal progenitors were highly competent to initiate MLL-ENL–driven AML, we tested whether Lin28b, a fetal master regulator, could accelerate leukemogenesis. Surprisingly, Lin28b suppressed AML initiation rather than accelerating it. This may explain why MLL rearrangements often occur before birth in human infant leukemia patients, but transformation usually does not occur until after birth, when Lin28b levels decline. Our findings show that the efficiency of MLL-ENL–driven AML initiation changes through the course of pre- and postnatal development, and developmental programs can be manipulated to impede transformation.

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