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įor many years, neither "apoptosis" nor "programmed cell death" was a highly cited term. He shared the prize with Boston biologist H. Kerr received the Paul Ehrlich and Ludwig Darmstaedter Prize on March 14, 2000, for his description of apoptosis. Kerr, Wyllie and Currie credited James Cormack, a professor of Greek language at University of Aberdeen, with suggesting the term apoptosis. Kerr had initially used the term programmed cell necrosis, but in the article, the process of natural cell death was called apoptosis. In 1972, the trio published a seminal article in the British Journal of Cancer. Following the publication of a paper describing the phenomenon, Kerr was invited to join Alastair Currie, as well as Andrew Wyllie, who was Currie's graduate student, at the University of Aberdeen. While studying tissues using electron microscopy, John Kerr at the University of Queensland was able to distinguish apoptosis from traumatic cell death. However, it was not until 1965 that the topic was resurrected. In 1885, anatomist Walther Flemming delivered a more precise description of the process of programmed cell death. German scientist Carl Vogt was first to describe the principle of apoptosis in 1842. Main article: History of apoptosis research Some factors like Fas receptors and caspases promote apoptosis, while some members of the Bcl-2 family of proteins inhibit apoptosis. Excessive apoptosis causes atrophy, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer. In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in a wide variety of diseases. The two pathways both activate initiator caspases, which then activate executioner caspases, which then kill the cell by degrading proteins indiscriminately. Both pathways induce cell death by activating caspases, which are proteases, or enzymes that degrade proteins. Weak external signals may also activate the intrinsic pathway of apoptosis. In the intrinsic pathway the cell kills itself because it senses cell stress, while in the extrinsic pathway the cell kills itself because of signals from other cells. Apoptosis can be initiated through one of two pathways. īecause apoptosis cannot stop once it has begun, it is a highly regulated process. Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytes are able to engulf and remove before the contents of the cell can spill out onto surrounding cells and cause damage to them. For example, the separation of fingers and toes in a developing human embryo occurs because cells between the digits undergo apoptosis. In contrast to necrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis is a highly regulated and controlled process that confers advantages during an organism's life cycle.
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For an average human child between eight and fourteen years old, each day the approximate loss is 20 to 30 billion cells. The average adult human loses between 50 and 70 billion cells each day due to apoptosis. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, DNA fragmentation, and mRNA decay. Biochemical events lead to characteristic cell changes ( morphology) and death. Apoptosis (from Ancient Greek: ἀπόπτωσις, romanized: apóptōsis, lit.'falling off') is a form of programmed cell death that occurs in multicellular organisms and in some eukaryotic, single-celled microorganisms such as yeast.