The concept Fetal Alcohol Syndrome (FAS) refers to a set of birth defects that occur in children born to mothers who abused alcohol during pregnancy. The alcohol-induced defects include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing central nervous system (CNS). FAS is the most serious condition physicians group under the heading of Fetal Alcohol Spectrum Disorders, which also includes Alcohol-Related Birth Defects, like alcohol-induced congenital cardiac defects that are unrelated to a diagnosis of FAS, and Alcohol-Related Neurodevelopmental Disorders, which occur in the absence of any facial birth defects or growth delays. The severity of birth defects associated with FAS can vary depending on the intensity, duration, and frequency of exposure to alcohol during gestation. In addition to these dose-related concerns, maternal factors such as the mother's genetics or how quickly she metabolizes alcohol, and the timing of exposure during prenatal development also impact alcohol-induced abnormalities. As birth defects and anomalies can arise when pregnant women consume alcohol, alcohol is a teratogen, an environmental agent that negatively impacts the course of normal embryonic or fetal development.

When scientists discovered a 3.3 million-year-old skeleton of a child of the human lineage (hominin) in 2000, in the village of Hadar, Ethiopia, they were able to study growth and development of Australopithecus afarensis, an extinct hominin species. The team of researchers, led by Zeresenay Alemseged of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, named the fossil DIK 1-1 and nicknamed it Dikika baby after the Dikika research site. The Dikika fossil preserves much of the skull, including the jaw and teeth, which enabled scientists to study the teeth microstructures and to reconstruct the pace at which individuals of the hominin A. afarensis developed.

Dinosaur egg parataxonomy is a classification system that organizes dinosaur eggs by descriptive features such as shape, size, and shell thickness. Though egg parataxonomy originated in the nineteenth century, Zi-Kui Zhao from Beijing, China, developed a modern parataxonomic system in the late twentieth century. Zhao's system, published in 1975, enabled scientists to organize egg specimens according to observable features, and to communicate their findings. The eggshell protects the developing embryo, enables gas exchange between the embryo and the environment external to the egg, and the internal components of the egg provide nutrients for the embryo. Those external and internal features that support a developing embryo leave their mark on eggshells. Dinosaur egg parataxonomy classifies those characteristics and provides insight into dinosaur egg-laying behaviors, reproductive physiology, and embryonic development.

Androgen Insensitivity Syndrome (AIS) is a human disorder in which an individual's genetic sex (genotype) differs from that individual's observable secondary sex characteristics (phenotypes). A fetus with AIS is genetically male with a 46,XY genotype. The term 46,XY refers to the chromosomes found in most cells of the fetus. Most cells have a total of 46 autosomes, or non-sex chromosomes, and a pair sex chromosomes, XX for genetic females, or XY for genetic males. Due to a defect on the androgen receptor gene (AR) located on the X chromosome, a fetus with AIS cannot process male sex hormones or androgens. The effect on the fetus is that, compared to genetically male fetuses without AIS, it doesn't develop normal male phenotypes. The resistance to androgens affects all of the fetus's organs during embryonic development and during puberty. Although genetically male, persons with AIS can be socially raised as either female or male (sex-of-rearing) yet identify with a gender discordant with their sex-of rearing. AIS and other states of intersexuality challenge physicians, scientists, and society to evaluate definitions of sex.

The one gene-one enzyme hypothesis, proposed by George Wells Beadle in the US in 1941, is the theory that each gene directly produces a single enzyme, which consequently affects an individual step in a metabolic pathway. In 1941, Beadle demonstrated that one gene in the bread mold Neurospora controlled a single, specific chemical reaction in Neurospora, which one enzyme controlled. In the 1950s, the theory that genes produce enzymes that control a single metabolic step was dubbed the one gene-one enzyme hypothesis by Norman Horowitz, a professor at the California Institute of Technology (Caltech) and an associate of Beadle's. This concept helped researchers characterize genes as chemical molecules, and it helped them identify the functions of those molecules.

James Graves Wilson's six principles of teratology, published in 1959, guide research on teratogenic agents and their effects on developing organisms. Wilson's six principles were inspired by Gabriel Madeleine Camille Dareste's five principles of experimental teratology published in 1877. Teratology is the study of birth defects, and a teratogen is something that either induces or amplifies abnormal embryonic or fetal development and causes birth defects. Detailed in his 1973 monograph, Environment and Birth Defects, Wilson's principles helped scientists research teratogens experimentally.

Angelman syndrome is a disorder in humans that causes neurological symptoms such as lack of speech, jerky movements, and insomnia. A human cell has two copies of twenty-three chromosomes for a total of forty-six-one copy from its mother and one from its father. But in the case of Angelman syndrome, the maternal chromosome numbered 15 has a mutation or deletion in its DNA and a gene on the paternal chromosome 15 is inactivated in some parts the brain. The result is the paternal gene is silenced during development of the sperm, which is called genetic imprinting. Angelman syndrome was one of the first disorders described as caused by genetic imprinting.

Purkinje cells, also called Purkinje neurons, are neurons in vertebrate animals located in the cerebellar cortex of the brain. Purkinje cell bodies are shaped like a flask and have many threadlike extensions called dendrites, which receive impulses from other neurons called granule cells. Each cell also has a single projection called an axon, which transmits impulses to the part of the brain that controls movement, the cerebellum. Purkinje cells are inhibitory neurons: they secrete neurotransmitters that bind to receptors that inhibit or reduce the firing of other neurons. Purkinje cells were the first neuronal cells identified. Researchers study the embryonic development of Purkinje cells to elucidate how they function in various mechanisms in the body.

Vitamin A (retinol) is an essential vitamin in the daily functioning of human beings that helps regulate cellular differentiation of epithelial tissue. Studies have shown that an excess of vitamin A can affect embryonic development and result in teratogenesis, or the production of birth defects in a developing embryo. Excess intake of vitamin A and retinoids by pregnant women often results malformations to fetuses' skulls, faces, limbs, eyes, central nervous system. Additionally, doctors often use derivatives of vitamin A, known as retinoids, as medicine to treat a number of skin conditions and carcinomas, the most common form of human cancers.

The Hayflick Limit is a concept that helps to explain the mechanisms behind cellular aging. The concept states that a normal human cell can only replicate and divide forty to sixty times before it cannot divide anymore, and will break down by programmed cell death or apoptosis. The concept of the Hayflick Limit revised Alexis Carrel's earlier theory, which stated that cells can replicate themselves infinitely. Leonard Hayflick developed the concept while at the Wistar Institute in Philadelphia, Pennsylvania, in 1965. In his 1974 book Intrinsic Mutagenesis, Frank Macfarlane Burnet named the concept after Hayflick. The concept of the Hayflick Limit helped scientists study the effects of cellular aging on human populations from embryonic development to death, including the discovery of the effects of shortening repetitive sequences of DNA, called telomeres, on the ends of chromosomes. Elizabeth Blackburn, Jack Szostak and Carol Greider received the Nobel Prize in Physiology or Medicine in 2009 for their work on genetic structures related to the Hayflick Limit.