Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading fetal alcohol spectrum disorders (FASD). Fetal alcohol syndrome (FAS) is the most severe combination of these defects under this heading, and is characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system (CNS). The developing brain is particularly vulnerable to the toxicity of ethanol, given the broad time frame of susceptibility from neurulation, when the neural tube is formed, all the way through to birth. The cerebellum is an area of the brain particularly vulnerable to prenatal ethanol exposure. Mechanisms proposed for this drastic reduction in brain cells include apoptosis, oxidative stress, and damage to the radial glia stem cell progenitor pool. Physical dexterity, coordination, and visuospatial processing are all affected by these stressors, and eyeblink classical conditioning tests have proven that ethanol-induced damage goes beyond motor coordination by permanently impacting learning and memory.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system. The pattern of facial defects that occur as a result of ethanol exposure during development primarily affects the midline of the face, altering morphology of the eyes, nose, and lips. Ethanol damage to cranial neural crest cells (CNCC) early in embryonic development is responsible for these minor midline abnormalities. Regulation of the gene sonic hedgehog (shh) during this period of development has been observed to rescue these ethanol-affected CNCC from fated cell death, an association that has not yet been examined as it applies to human cells.

After becoming chief pathologist at the University of Wisconsin-Madison Wisconsin Regional Primate Center in 1995, James A. Thomson began his pioneering work in deriving embryonic stem cells from isolated embryos. That same year, Thomson published his first paper, "Isolation of a Primate Embryonic Stem Cell Line," in Proceedings of the National Academy of Sciences of the United States of America, detailing the first derivation of primate embryonic stem cells. In the following years, Thomson and his team of scientists - Joseph Itskovitz-Eldor, Sander S. Shapiro, Michelle A. Waknitz, Jennifer J. Swiergiel, Vivienne S. Marshall, and Jeffry M. Jones - advanced their work with embryonic stem cells, eventually isolating and culturing human embryonic stem cells. Their work with human embryos was reported in the 1998 Nature article "Embryonic Stem Cell Lines Derived from Human Blastocysts."

George Linius Streeter was born on 12 January 1873 in Johnstown, New York, to Hannah Green Anthony and George Austin Streeter. He completed his undergraduate studies at Union College in 1895 and received his MD degree from the College of Physicians and Surgeons of Columbia University in 1899. At Columbia, Professor George S. Huntington sparked Streeter's interest in anatomy, and Streeter also interned at Roosevelt Hospital in New York City. He then went on to Albany to teach anatomy at the Albany Medical College and to work with neurologist Henry Hun. In 1902 he studied with Ludwig Edinger at Frankfurt and with Wilhelm His at Leipzig. After working with His, Streeter shifted his focus to embryology, particularly the development of the human nervous system.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) is part of this group and was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities and defects of the central nervous system (CNS). The CNS is particularly vulnerable to the effects of ethanol during prenatal development. Severe exposure correlates with gross morphological abnormalities and an overall decrease in white matter. Mechanisms for how ethanol affects the development of the CNS are complicated, but damage to neural stem cell progenitor pools that give rise to neurons and glia is strongly suspected to be a major factor. Damage to this population of cells at any point during CNS development can result in abnormalities in the formation and maturation of these cells, from the initial differentiation through the maturation of neuronal networks. This damage can lead to a wide variety of cognitive deficiencies, functional impairments, and behavioral problems depending on the area of the brain impacted by prenatal ethanol exposure.

The term Fetal Alcohol Syndrome (FAS) was first published in 1973 in an article published in the British medical journal The Lancet. In that article, a group of pediatricians and psychiatrists at the University of Washington Medical School helped to define the morphological defects and developmental delays that can affect children born to alcoholic mothers. Those observations include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing brain that can result in behavioral, learning, and cognitive abnormalities.

In the US, one in 1000 births is affected by neural tube defects (NTD). A neural tube defect is a birth defect involving the malformation of body features associated with the brain and spinal cord. An NTD originates from and is characterized by incomplete closure of the neural tube, which is an organizer and precursor of the central nervous system. In humans, incomplete closure of the neural tube during embryonic development results in anatomical abnormalities such as anencephaly (a severe lack of skull and brain), hydranencephaly (cerebral hemispheres replaced with sacs of cerebrospinal fluid), spina bifida occulta (incompletely closed lower spinal cord), iniencephaly (severe retroflexed head and spinal defects), and encephalocele (a sac-like protrusion from an opening somewhere along the midline of the skull).

The development of the obstetric ultrasound has allowed physicians and embryologists to obtain a clear picture of the developing human embryo and fetus during pregnancy. Obstetric ultrasonography, often referred to as ultrasound, is a technology that uses sound waves to produce images of structures inside the human body. A handheld probe emits sound waves, which are reflected back by the different structures within the body. These reflected sound waves are converted into electric signals that are detected by a transducer, which then produces two-dimensional images that can be interpreted by medical professionals. Ultrasound technology has become a sophisticated, high-resolution diagnostic imaging tool used widely in medicine, especially obstetrics.

Maternal consumption of alcohol (ethanol) can result in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The eye and ocular system development is particularly susceptible to the effects of prenatal alcohol exposure and can result in visual impairment or blindness.

Parasitic twins, a specific type of conjoined twins, occurs when one twin ceases development during gestation and becomes vestigial to the fully formed dominant twin, called the autositic twin. The underdeveloped twin is called parasitic because it is only partially formed, is not functional, or is wholly dependent on the autositic twin. In most cases, the phenotype of parasitic twins is one normal functioning individual with extra appendages or organs, leading to questions about whether or not the additional limbs and organs are in fact another person or just a mutation of the individual's body. Researchers think that parasitic twins result from mechanisms similar to those that produce Vanishing Twin Syndrome. On a developmental continuum with vanishing twin syndrome on one end and developmentally normal twins on the other, researchers propose that the patterns of conjoined twins fall in the middle.