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While colchicine is not used to treat cancer in humans, it is commonly used to treat acute attacks of gout. [26] Colchicine is an anti-inflammatory drug that has been in continuous use for more than 3000 years. Colchicine is an oral drug, known to be used for treating acute gout and preventing acute attacks of familial Mediterranean fever (FMF).
In the United States, several hundred cases of colchicine toxicity are reported annually, about 10% of which end with serious morbidity or mortality. Many of these cases are intentional overdoses, but others were accidental; for example, if the drug were not dosed appropriately for kidney function. Most cases of colchicine toxicity occur in adults.
Spindle poisons, in contrast, inhibit kinetochores during mitosis and prevent them from forming proper attachments to spindle microtubules. Permanent activation of the SAC ensues along with a mitotic arrest that lasts several hours. These cells will either exit mitosis by a different pathway not normal to mitosis or they will apoptose. [3]
For example, the hydra reproduces asexually by budding. The cells at the surface of hydra undergo mitosis and form a mass called a bud. Mitosis continues in the cells of the bud and this grows into a new individual. The same division happens during asexual reproduction or vegetative propagation in plants.
Demecolcine is used for scientific research in cells. It is used in a variety of ways, however, until recently, was used mostly for the study of mitosis in cells. For example, microtubules are necessary for the splitting of cells. More importantly, the movement of chromosomes during the M phase.
Cytochalasin B, the name of which comes from the Greek cytos (cell) and chalasis (relaxation), [1] is a cell-permeable mycotoxin.It was found that substoichiometric concentrations of cytochalasin B (CB) strongly inhibit network formation by actin filaments.
A cell that has been treated with taxol and had a catastrophic mitosis. The cell has become multinucleated after an unsuccessful mitosis. Mitotic catastrophe has been defined as either a cellular mechanism to prevent potentially cancerous cells from proliferating or as a mode of cellular death that occurs following improper cell cycle progression or entrance.
An example that reveals the interaction of the multiple negative and positive feedback loops is the activation of cyclin-dependent protein kinases, or Cdks14. Positive feedback loops play a role by switching cells from low to high Cdk-activity. The interaction between the two types of loops is evident in mitosis.