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Mechanisms and Hormones of Parturition Study Guide

This guide delves into the critical role of the placenta in fetal development. It covers how the placenta functions as a sensor for nutrients and oxygen, and the consequences of environmental factors such as hypoxia, maternal stress, and inflammation on placental programming. The guide also examines the concept of sexual dimorphism in placental responses and the long-term health implications for the offspring, including the developmental origins of chronic diseases.

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Foundations of DOHaD and Developmental Programming

Introduction to the DOHaD Paradigm

The Developmental Origins of Health and Disease concept proposes that environmental factors during early life development can have long-lasting effects on an individual's health and disease risk in adulthood.

developmental plasticity
developmental programming
critical windows of plasticity
intrauterine environment
chronic disease prevalence
non-communicable diseases
malnutrition

Environmental Influences on Human Development

Nutrition and other environmental influences impact human development and the developmental origins of health and disease across the human lifespan.

environmental influences
human development
nutrition
developmental origins of health and disease
genetics
epigenetics
endocrine function

Introduction to DOHaD and Barker Hypothesis

The developmental origins of health and disease (DOHaD) explores how environmental factors during critical windows of plasticity influence lifelong health and disease profiles.

Barker hypothesis
Developmental origins of health and disease (DOHaD)
Fetal origins of adult disease (FOAD)
Developmental plasticity
Developmental programming
Critical windows of vulnerability
Predictive Adaptive Response (PAR) Model
Developmental Constraints Model
Gene-environment interactions (GXE)
Reaction norm
Dutch Hunger Winter
Low birthweight
Type 2 diabetes
Metabolic and cardiovascular disease
Nutritional programming
Phenotypic plasticity

Thrifty Phenotype and Developmental Mismatch

The thrifty phenotype hypothesis explains how nutritional programming during critical windows of development causes lasting changes to body structure and function, potentially leading to developmental mismatch and metabolic disorders.

Thrifty phenotype hypothesis
Nutritional programming
Developmental plasticity
Predictive adaptive response
Evolutionary mismatch
Developmental mismatch
Metabolic programming
Type 2 diabetes
Insulin resistance
Metabolic syndrome
Endocrine pancreas development

Introduction to Developmental Origins of Health and Disease

Adversity in early development and postnatal challenges influence the pathogenesis of disease and noncommunicable disease risks throughout the human lifecourse.

Multiple Hits Hypothesis
Developmental Origins of Health and Disease (DOHaD)
Critical Periods
Developmental Plasticity
Predictive Adaptive Responses
Epigenetic Mechanisms
Transgenerational Effects
Life Course Approach
Social Determinants of Health
Noncommunicable Disease (NCD) Risk

Nutrigenomics and Epigenetics in Nutrition

Nutrigenomics is the study of the effects of foods and food constituents on gene expression and the epigenome.

Nutrigenomics
Epigenetics
Gene expression
DNA methylation
Methyl-donating nutrients
Folic acid
B vitamins
Chronic disease
Nutritional genomics

Topic 1

DOHaD Mechanisms and Epigenetic Programming

Maternal behavior and tactile stimulus regulate the epigenome, specifically affecting DNA methylation and glucocorticoid receptor expression in the hippocampus.

Developmental origins of health and disease (DOHaD)
Epigenetic programming
Maternal behavior
DNA methylation
Glucocorticoid receptor (GR) gene promoter
Hippocampus
Histone acetylation
Transcription factor (NGFI-A) binding
Tactile stimulus

Placental Development, Physiology, and Programming

Mechanisms and Hormones of Parturition

Parturition involves sequential changes within the myometrium, decidua, and cervix driven by hormonal mechanisms including progesterone withdrawal, estrogen increases, oxytocin, prostaglandins, and HPA axis activation.

Parturition
Labor diagnosis
Functional progesterone withdrawal
Estrogen bioavailability
Myometrial responsiveness
Corticotrophin releasing hormone (CRH)
Uterine stretch
Progesterone receptor expression
Oxytocin
Prostaglandins
Cervical ripening
Glucocorticoid production

Placenta Programming and Developmental Outcomes

Environmental exposures can alter placental structure and function, impacting nutrient and oxygen delivery to the fetus and influencing long-term health outcomes.

placental programming
developmental programming
placenta as a nutrient sensor
placenta as an oxygen sensor
placenta as a GC barrier
placenta as an inflammation mediator
sexual dimorphism
placental plasticity
placental size and efficiency
fetal growth restriction
placental dysfunction
maternal undernutrition
gestational diabetes mellitus
nutrient transporters

Placenta Programming and Hypoxia Effects

Hypoxia acts as an oxygen sensor and main cause of fetal growth restriction through morphological changes and altered nutrient transporter signalling.

Hypoxia
Fetal growth restriction
Placental nutrient transporter expression
Villous vascularization
mTOR signaling
HIF-1 transcription factor
Oxygen homeostasis
Glucocorticoids
Maternal stress

The Placental Glucocorticoid Barrier

The placenta regulates fetal exposure to cortisol and other glucocorticoids to manage appropriate fetal development and prevent inappropriate fetal development.

Glucocorticoid Barrier
Cortisol
Cortisone
Appropriate fetal development
Inappropriate fetal development
Fetal growth restriction
Pre-term birth
Chronic disease in later life
Hypotension

Placenta as an Inflammation Mediator

Placental inflammation from infectious agents or non-infectious insults affects fetal programming and developmental origins of health and disease.

Fetal programming
Placental inflammation
Classical inflammatory response
Meta-inflammation
Smoldering inflammation
TORCH infections
Zika virus transmission
Vertical transmission
Epigenetic modification
Fetal growth restriction

Sexual Dimorphism in Placental Programming

Sexual dimorphism refers to biological differences in appearance, physiology, or behavior between males and females that affect placental function, development, and response to environmental insults.

Sexual dimorphism
Placental function
Gene expression profiles
Trophoblast differentiation
Maternal high fat diet
Metabolic adaptations
Sex chromosomes
X-inactivation
Epimutations
Placental methylation patterns
Gonadal sex hormones

Placental Development and Circulation

Placental development milestones
Feto-placental circulation
Utero-placental circulation
Maternal-fetal exchange
Selective barrier functions
Syncytiotrophoblast
Cytotrophoblast
Intervillous spaces
Spiral arteries
Decidual plate
Endometrial veins

Implantation and Invasion Disorders

This content discusses implantation and invasion disorders including placenta previa and placenta accreta.

Placenta previa
Low lying placenta
Marginal placenta
Complete placenta previa
Placenta accreta
Placenta increta
Placenta percreta
Decidua basalis
Hemorrhage
Hysterectomy
C-section delivery

Maternal-Fetal Exchange and Placental Physiology

This content explores maternal-fetal exchange through various transport mechanisms including diffusion, facilitated diffusion, osmosis, active transport, and vesicular transport to support placental functions and fetal nutrition.

Maternal-fetal exchange
Placental physiology
Simple diffusion
Facilitated diffusion
Osmosis
Active transport
Vesicular transport
Endocytosis
Exocytosis
Glucose transport
Amino acid transport
Fatty acid transport
Macronutrients
Syncytiotrophoblast

Placenta Development and Endocrine Functions

The placenta regulates maternal hormones, promotes fetal growth, and ensures respiratory function through various endocrine secretions.

Progesterone
Estrogen
Estradiol
Estriol
Placental Lactogen
Placental Growth Hormone
Leptin
Corpus luteum
Myometrial contractions
Mammary gland development
Maternal insulin resistance
Fetal growth
Respiratory function of placenta

Placental Functions and the Placental Barrier

The placenta serves as a barrier protecting the fetus from infection, xenobiotics, and elevated cortisol while facilitating fetal circulation, immunity, and excretory functions.

fetal circulation
ductus venosus
ductus arteriosus
placental barrier
teratogens
congenital infection
glucocorticoids
xenobiotics
ABC transporters
cytochrome P450 system
maternal antibodies
FcRn receptor
excretory functions

Pregnancy, Obstetrical Complications, and Offspring Health

Pregnancy and Obstetrical Complications

This content covers measuring health in pregnancy, fetal health metrics, neonatal health metrics, and various obstetrical complications including pre-term birth, fetal growth restriction, and preeclampsia.

Fetal health metrics
Neonatal health metrics
APGAR evaluation
Pre-term birth
Fetal growth restriction
IUGR/FGR
Preeclampsia
HELLP Syndrome
Gestational diabetes
Placental function
Developmental programming

Gestational Diabetes and Obstetrical Complications

This content examines gestational diabetes, its pathophysiology involving insulin resistance and hyperglycemia, and its associated maternal and neonatal complications.

Gestational diabetes
Hyperglycemia
Insulin resistance
Macrosomia
Placental hormones
Leptin
Adiponectin
Pre-eclampsia
Eclampsia
Maternal hemorrhage
Type 2 diabetes mellitus
Cardiovascular disease
Environmental risk factors
Socioeconomic risk factors

Impact of ART and Paternal Age

The sources discuss how culture media, assisted reproductive technology (ART), and advanced paternal age impact pregnancy outcomes, birthweight, and offspring health.

culture media impact
pregnancy rates
birthweight distributions
assisted reproductive technology (ART) outcomes
vascular dysfunction in IVF children
seminal fluid microbiome
advanced paternal age
epigenetic changes
autism risk
schizophrenia risk

In Utero BaP Exposure Effects

In utero exposure to BaP affects male and female offspring reproductive parameters and induces ovarian mutations.

In utero exposure
Transplacental exposure
Fetal organogenesis
Male offspring reproductive parameters
Sperm development and function
Ovarian mutations
Oogenesis
Spermatogenesis
Mutagenesis

Gametogenesis, Fertilization, and Reproductive Technologies

Gametogenesis and Fertilization Processes

The membrane fusion process, fast block, slow block, and fusion of the pronuclei occur during fertilization.

membrane fusion
attachment
membrane apposition
lipid mixing
fast block
slow block
cortical reaction
fertilization membrane
meiosis II
pronuclei
sperm chromatin decondensation
pronuclear fusion

Spermatogenesis and Male Gamete Development

This topic covers the processes of spermatogenesis, including the roles of Sertoli and Leydig cells, hormonal regulation, and the maturation of sperm cells.

spermatogenesis
blood-testis barrier
Sertoli cells
Leydig cells
testosterone
LH
FSH
spermatogonia
meiosis
spermiogenesis
spermiation
capacitation
semen composition

Spermatogenesis, Infertility, and Epigenetic Modifications

male infertility factors
sperm concentration
sperm motility
sperm morphology
spermatogenesis
chromosomal abnormalities
aneuploidy
non-disjunction
epigenetic reprogramming
chromatin organization
DNA methylation
protamines
histones
post-translational modification

Gametogenesis, Oogenesis, and Human Fertilization

This topic explores the biological processes of oogenesis, the structural features of the ovum, and the sequential stages of human fertilization.

Spermatogenesis
Oogenesis
Primordial germ cells
Primary oocytes
Polar body
Ovum structural features
Zona pellucida
Granulosa cells
Antrum
Corpus luteum
Aneuploidy
Epigenetics
DNA methylation
Histone acetylation
Sperm preparation

Pregnancy and the Prenatal Period

This lecture covers the prenatal period, including fertilization, implantation, the embryonic and fetal periods, and the process of organogenesis.

prenatal period
ontogenesis
conception
implantation
embryonic period
fetal period
organogenesis
gastrulation
germ layers
endoderm
mesoderm
placentation
placenta
maternal-fetal exchange
zygote
blastocyst
cortical reaction

Epigenetics and Cloning Processes

The manipulation of embryos for assisted reproduction or cloning involves reprogramming a somatic cell nucleus to an embryonic epigenetic state.

Epigenetics
Cloning
Somatic cell nuclear transfer
Embryo manipulation
Nuclear reprogramming
Gene expression
Epigenetic defects

Assisted Reproductive Technologies and Infertility

Medical options for infertility treatment including intrauterine insemination, in vitro fertilization, and intra-cytoplasmic sperm injection.

Assisted Reproductive Technologies (ART)
Ovulation induction
Intrauterine insemination (IUI)
In vitro fertilization (IVF)
Intra-cytoplasmic sperm injection (ICSI)
Third-party assisted ART
Mitochondrial DNA (mtDNA) screening
Mitochondrial replacement therapy
Egg rejuvenation
Spermbots
Oviductal fluid
Reproductive tract microbiomes
Fresh vs. frozen embryo transfer

Mechanisms of Epigenetics, Genetic Damage, and DNA Editing

Epigenetics and Human Disease

Epigenetic modifications and dysregulation contribute to the development of various human pathologies, including diabetes, mental health conditions, neurodegenerative diseases, autoimmunity, cancer, and aging.

DNA methylation
Histone modification
Non-coding RNAs
Fragile X syndrome
Schizophrenia
Autoimmune diseases
Cancer oncogenes and tumor suppressor genes
Epigenetic drift
Sirtuins
Epigenetic drug discovery
DNA methyltransferase inhibitors
CRISPR/Cas approach

Epigenetics in Development, Health, and Aging

Epigenetic mechanisms including DNA methylation, histone modification, and non-coding RNAs regulate gene expression and chromatin alterations throughout the human life cycle, influencing developmental programming, disease, and cellular aging.

DNA methylation
Histone modification
Non-coding RNAs
Genetic imprinting
X-chromosome inactivation
Pluripotent stem cells
Somatic cell differentiation
Paternal and maternal genome demethylation
Epigenetic modifications and disease
Environmental exposures and nutrition
Histone modifications
DNA methyltransferases
Histone acetyltransferases
CpG islands
One-carbon metabolism
S-adenosylmethionine
Long non-coding RNA

Mechanisms of Epigenetic Modifications and Chromatin

Epigenetic modifications such as histone modification and DNA methylation influence gene expression by altering the structure of chromatin.

Epigenetic modifications
Histone modification
DNA methylation
Chromatin structure
Gene expression regulation
Nucleosomes
Histone acetylation
Histone code hypothesis
Chromatin remodeling

Environmental and Dietary Regulation of Development

Biological development and phenotypic plasticity are regulated by temperature, hormones, and diet-induced developmental changes.

aromatase activity
temperature dependent sex determination
castes specification in honey bees
royal jelly
TOR and MAPK pathways
juvenile hormone
Dnmt3
methylated DNA

Types of Genetic Damage and Alterations

This content explains hereditary and acquired mutations, chromosomal abnormalities including aneuploidy, and various types of DNA and gene alterations.

Hereditary mutations
Acquired mutations
Chromosomal abnormalities
Aneuploidy
Trisomy
Monosomy
Meiosis errors
DNA mutations
Silent mutations
Nonsense mutations
Missense mutations
Frameshift mutations
Gene alterations
Trinucleotide-repeat mutations
Rare diseases

Genetic Damage and Autism Mutations

Somatic mutation
Germline mutation
Somatic mosaicism
De novo mutations
Copy number variants
Deletions
Duplications
Inherited variants
Polygenic variants
Epigenetic and regulatory changes
Paternal germline

Parental Age and Genetic Damage

This topic explores the relationship between parental age, environmental mutagens, and germline mutations in offspring.

maternal age effect
paternal age effect
genome replication hypothesis
de novo mutations
Down syndrome
aneuploidy
neurodevelopmental outcomes
selfish mutations
spermatogonia
environmental mutagens
polyaromatic hydrocarbons
minisatellites
microsatellite mutation frequencies
benzoapyrene
ethylnitrosourea

Mechanisms and Disorders of Genomic Imprinting

Genomic imprinting is an epigenetic process involving DNA methylation and histone methylation that results in parental-specific gene expression.

Genomic imprinting
Epigenetic process
DNA methylation
Histone methylation
Differently methylated region (DMR)
Germline DMR
Somatic DMR
Epigenetic reprogramming
Prader-Willi syndrome
Angelman syndrome
Chromosome 15q11-q13

Mechanisms of X-Chromosome Inactivation

dosage compensation
X-chromosome inactivation
Xist gene
Tsix gene
long noncoding RNA
transcriptional silencing
sex determination
SRY gene
genes that escape X-inactivation
autoimmunity

CRISPR/Cas9 Technology and DNA Editing

CRISPR-Cas9 is a unique technology that enables geneticists and medical researchers to edit parts of the genome by removing, adding or altering sections of the DNA sequence.

CRISPR/Cas9 editing
Cas9 nuclease
Off-target activity
Bacterial CRISPR-Cas9 antiviral defense system
Germline genetic modification
Somatic mutations
Viral vectors
CCR5 gene
Mosaicism

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