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Category Archives: Apoptosis - Part 2

Liver cell death: Overview of apoptosis (Part 2)

undergo apoptosis in the C elegans modelPerhaps more important, the work of the 2002 Nobel Prize winners in Medicine and Physiology clearly demonstrated that a component of the genome is required for some forms of apoptosis to occur. In the early 1960s, Dr Sydney Brenner chose a small nematode (Caenorhabditis elegans) to study fundamental questions regarding cell differentiation and organ development that he believed would be difficult to answer in higher animals. In the 1970s, John E Sulston discovered that a precise number of cells died at a predictable stage of the worm’s development. In 1986, Robert Horvitz identified the first genes that were essential for these cells to die. Thanks to their work, the key enzymes involved in the regulation of apoptosis have now been identified not only in worms but also in all other higher animals, including humans. Continue reading

Liver cell death: Overview of apoptosis (Part 1)

The word ‘apoptosis’ is derived from the Greek ‘apo’ (off) and ‘ptosis’ (falling). This neologism was chosen because of the analogy between this type of cell death and what happens to leaves when they fall from trees. The comparison is indeed very appropriate as we understand more thoroughly what happens to apoptotic cells. The word was first used in 1972 by Kerr et al, who described the morphological characteristics of a particular form of cell death. Kerr was a liver pathologist who had earlier reported that necrosis could sometimes be accompanied by cell shrinkage, in opposition to the dogma that an increase in cell volume was one of the hallmarks of this form of cell death. The publication of further key articles in the 1980s led to an explosion of enthusiasm for the study of apoptosis. In 1980, Wyllie discovered that apoptosis was accompanied by a nonrandom form of DNA fragmentation that he postulated was due to a cellular endonuclease (an enzyme whose function is to cut nucleic acids). Continue reading

Liver cell death: CLINICAL SCENARIO

human immunodeficiency virusA 44-year-old, human immunodeficiency virus (HIV)-infected man is referred for evaluation of elevated serum liver enzymes. Ten years ago, he contracted acute hepatitis B, which has subsequently cleared completely. He is a known carrier of the hepatitis C virus (HCV). He has been treated for HIV with zidovudine, lamivudine and efavirenz for one year. Three months ago, measurement of the HIV viral load showed that viral replication was under control. However, antiviral treatment was stopped four weeks ago when aspartate transaminase and alanine transaminase levels rose from 40 to greater than 100 U/L. The patient does not drink alcohol and is not obese. Currently, the aspartate transaminase level is 396 U/L, the alanine transaminase level is 460 U/L and the alkaline phosphatase level is 119 U/L. An abdominal ultrasound reveals normal liver echogenicity without splenic enlargement. A liver biopsy shows significant inflammation consistent with a diagnosis of chronic, active hepatitis C. The activity index is 12/18 and the fibrosis score is I/IV. Inflammation is especially prominent in the liver lobules with abundant apoptotic figures. Take advantage of this unique opportunity to pay less money and get yourself a trusted pharmacy where you can always enjoy a chance to order antibiotics online buy here and be sure you will enjoy lowest prices online. Continue reading

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