Embryo Project Encyclopedia Articles

Breast augmentation involves the use of implants or fat tissue to increase patient breast size. As of 2019, breast augmentation is the most popular surgical cosmetic procedure in the United States, with annual patient numbers increasing by 41 percent since the year 2000. Since the first documented breast augmentation by surgeon Vincenz Czerny in 1895, and later the invention of the silicone breast implant in 1963, surgeons have developed the procedure into its own specialized field of surgery, creating various operating techniques for different results. By having varied incisions, implant placements, and improved ways of treating surgery-related complications, advanced technology has enabled women to undergo breast augmentations for aesthetic, medical, or reconstructive reasons. Trans women may also benefit from breast augmentations. Having the option of a breast augmentation gives women more control over their physical appearance, which may improve their self-image and boost their confidence.

In the 1960s, two plastic surgeons from the United States, Thomas Dillon Cronin and Frank Judson Gerow, collaborated with the Dow Corning Corporation, which specialized in silicone products, to create the first silicone breast implant. Surgeons used the implant, named the Cronin-Gerow implant, to improve the look of a woman’s breasts, by correcting for asymmetry, augmenting the size, or creating a more uplifted profile. Surgeons began widely using the breast implant almost immediately after it reached the US market in 1964, and breast augmentation quickly became one of the most popular cosmetic surgeries in the country. The creation of a silicone breast implant not only established a new branch of cosmetic surgery, but it also enabled women with breast cancer to receive reconstructions to improve their aesthetic appearance after cancer treatment and removal of the cancerous breast tissues.

Telomeres are sequences of DNA on the ends of chromosomes that protect chromosomes from sticking to each other or tangling, which could cause irregularities in normal DNA functions. As cells replicate, telomeres shorten at the end of chromosomes, which correlates to senescence or cellular aging. Integral to this process is telomerase, which is an enzyme that repairs telomeres and is present in various cells in the human body, especially during human growth and development. Telomeres and telomerase are required for normal human embryonic development because they protect DNA as it completes multiple rounds of replication.

Sir John Bertrand Gurdon further developed nuclear transplantation, the technique used to clone organisms and to create stem cells, while working in Britain in the second half of the twentieth century. Gurdon's research built on the work of Thomas King and Robert Briggs in the United States, who in 1952 published findings that indicated that scientists could take a nucleus from an early embryonic cell and successfully transfer it into an unfertilized and enucleated egg cell. Briggs and King also concluded that a nucleus taken from an adult cell and similarly inserted into an unfertilized enucleated egg cell could not produce normal development. In 1962, however, Gurdon published results that indicated otherwise. While Briggs and King worked with Rana pipiens frogs, Gurdon used the faster-growing species Xenopus laevis to show that nuclei from specialized cells still held the potential to be any cell despite its specialization. In 2012, the Nobel Prize Committee awarded Gurdon and Shinya Yamanaka its prize in physiology and medicine for for their work on cloning and pluripotent stem cells.

Carol Widney Greider studied telomeres and telomerase in the US at the turn of the twenty-first century. She worked primarily at the University of California, Berkeley in Berkeley, California.
She received the Nobel Prize in Physiology or Medicine in 2009, along with Elizabeth Blackburn and Jack Szostak, for their research on telomeres and telomerase. Telomeres are repetitive sequences of
DNA at the ends of chromosomes that protect chromosomes from tangling, and they provide some protection from mutations. Greider also studied telomerase, an enzyme that repairs telomeres. Without telomeres, chromosomes are subject to mutations that can lead to
cell death, and without telomerase, cells might not reproduce fast enough during embryonic development. Greider's research on telomeres helped scientists explain how chromosomes function within cells.

Telomerase is an enzyme that regulates the lengths of telomeres in the cells of many organisms, and in humans it begins to function int the early stages of embryonic development. Telomeres are repetitive sequences of DNA on the ends of chromosomes that protect chromosomes from sticking to each other or tangling. In 1989, Gregg Morin found that telomerase was present in human cells. In 1996, Woodring Wright and his team examined human embryonic cells and found that telomerase was active in them. Scientists manipulate telomerase in cells to give cells the capacity to replicate infinitely. Telomerase is also necessary for stem cells to replicate themselves and to develop into more specialized cells in embryos and fetuses.

Multiplex Automated Genome Engineering, or MAGE, is a genome editing technique that enables scientists to quickly edit an organism’s DNA to produce multiple changes across the genome. In 2009, two genetic researchers at the Wyss Institute at Harvard Medical School in Boston, Massachusetts, Harris Wang and George Church, developed the technology during a time when researchers could only edit one site in an organism’s genome at a time. Wang and Church called MAGE a form of accelerated evolution because it creates different cells with many variations of the same original genome over multiple generations. MAGE made genome editing much faster, cheaper, and easier for genetic researchers to create organisms with novel functions that they can use for a variety of purposes, such as making chemicals and medicine, developing biofuels, or further studying and understanding the genes that can cause harmful mutations in humans.

The Y-chromosome is one of a pair of chromosomes that determine the genetic sex of individuals in mammals, some insects, and some plants. In the nineteenth and twentieth centuries, the development of new microscopic and molecular techniques, including DNA sequencing, enabled scientists to confirm the hypothesis that chromosomes determine the sex of developing organisms. In an adult organism, the genes on the Y-chromosome help produce the male gamete, the sperm cell. Beginning in the 1980s, many studies of human populations used the Y-chromosome gene sequences to trace paternal lineages. In mammals, the Y-chromosomes contain the master-switch gene for sex determination, called the sex-determining region Y, or the SRY gene in humans. In most normal cases, if a fertilized egg cell, called a zygote, has the SRY gene, the zygote develops into an embryos that has male sex traits. If the zygote lacks the SRY gene or if the SRY gene is defective, the zygote develops into an embryo that has female sex traits.

Barbara McClintock conducted experiments on corn (Zea mays) in the United States in the mid-twentieth century to study the structure and function of the chromosomes in the cells. McClintock researched how genes combined in corn and proposed mechanisms for how those interactions are regulated. McClintock received the Nobel Prize in Physiology or Medicine in 1983, the first woman to win the prize without sharing it. McClintock won the award for her introduction of the concept of transposons, also called jumping genes. McClintock conceptualized some genetic material as not static in structure and order, but as subject to re-arrangement and may be altered during development.

Light therapy, also called phototherapy, exposes infants with jaundice, a yellowing of the skin and eyes, to artificial or natural light to break down the buildup of bilirubin pigment in the blood. Bilirubin is an orange to red pigment produced when red blood cells break down, which causes infants to turn into a yellowish color. Small amounts of bilirubin in the blood are normal, but when there is an accumulation of excess bilirubin pigment, the body deposits the excess bilirubin in the layer of fat beneath the skin. That accumulation of bilirubin causes the skin and the white areas of the eye to appear yellowed, a common symptom of jaundice. Buildup of bilirubin typically occurs when the immature liver of a newborn infant is unable to efficiently breakdown the bilirubin molecule into products that the body can excrete. High levels of bilirubin, a phenomenon called hyperbilirubinemia can be toxic and can lead to a brain dysfunction called kernicterus, which may result in permanent brain damage. The relative simplicity of phototherapy treatment has made effective neonatal jaundice treatment nearly universal, almost completely eliminating the risk of infant brain damage from hyperbilirubinemia.