Programmed cell death

body is quite amazing especially regarding cell injury. Throughout our lives the body cells continuously experience injury and repair and this is quite a fascinating subject to explore. The big question is what causes these injuries to the cells and what happens to it when it reaches a state of irreparability. All cells in our body sometimes experience stress which can be ranging from mild to severe and thus consequently ending in the injury to the cell. There are two major factors that determine

UV radiation, such as that from the sun can be very harmful. It has been shown to cause many different mutations within cells, leading to issues for the organism such as death or disease. One of the most prevalent sources of UV radiation for humans is the sun. It’s very important for us to know the extent of cellular damage that can be caused by this radiation, as to know how harmful the sun’s rays are to us as humans. One way that the damage caused by the suns radiation can be tested is through

Rubin, 2012). In the recent decade, neoplasms are incurably deleterious, formidable non-communicable diseases. A neoplasm presumably arises when a singly normal cell in a given tissue has dynamically accumulated irreversible genetic impairments and instability of such key genes. And these preposterous genes usually incurs a perversity of cell cycle, growth, proliferation, differentiation, survival as well as senescence because they have lost their regulatory functions (Hanahan and Weinberg, 2000; Kumar

sustained damage. Thus, it may be an important factor in aging. The gene has a very important location in the nucleus of our cells, where it binds directly to DNA. TP53 can arrest growth by holding the cell cycle at the G1/S regulation point on DNA damage recognition. If it holds the cell here for long enough, the DNA repair proteins will have time to fix the damage and the cell will be allowed to

Once any bleeding is under control, chemotaxis occurs and inflammatory cells migrate into the wound and promote the inflammatory phase, which is characterised by the successive influx of neutrophils, macrophages and lymphocytes. Neutrophils start with the critical task of destroying and removing bacteria, foreign particles and any remaining damaged tissue. This phagocytic activity is crucial as bacterial imbalance within acute wounds causes the wound to stop healing. Neutrophils are attracted to

chaacterised by decrease in B cell mass function and decrease in the sensitivity of insulin in the peripheral tissues. Beta cell dysfunctioning decrease the release of amylin and insulin in response to increased blood glucose levels and this is thought to be affected by misfolded amylin proteins where the cytotoxicity from amylin oligomers affects the function of islet beta cells via several mechanisms and affecting the signaling pathway and apoptosis of beta cells. Introduction: There are 2 major

Apoptosis helps shape organisms while eliminating cells that are no longer required. There are two types of programmed cell death: apoptosis and autophagy. Apoptotic cells release many signals during different many conditions. Apoptosis can remove potentially harmful cells. It also participates in morphogenesis, the origin and development of morphological characteristics. Some physical changes apoptosis cause include plasma membrane blebbing, permeabilization of the mitochondrial outer membrane

to genes that control the way our cells function (“What is Cancer?” National Cancer Institute). The genetic changes that subsidize cancer tend to affect three chief types of genes- proto-oncogenes, tumor suppressor genes, and DNA repair genes. These are the “drivers” of cancer. Cancer can appear and grow virtually anywhere in the body. Types of cancer are customarily named for the organs or tissues where they form. They can also be described by the types of cell that formed them. Although there

lysis and DMSO protocol, to demonstrate the effects Dexamethasome had on thymocytes DNA. The DMSO protocol is time efficient, involving the direct lysis of cells with dimethyl sulphoxide (DMSO), vortexing, adding of 2% SDS-TE buffer and centrifugation. While the lysis protocol is time consuming, involving the use of HBSS, the direct lysis of cells using a lysis buffer, incubation period, RNase A and centrifugation. Upon comparing both methods, the lysis protocol provided better results than the DMSO

with something called apoptosis or a programmed cell death, that kills the infected cells. But this is the first defense, which is called the Innate defense system (keep out, or quietly neutralizes, pathogens). The second defense is called the Adaptive immune system. When a white blood cell meets a new disease, it tries to meet with it and remember it from a threat to a friend. This ability to remember specific pathogens is one of the key differences between the adaptive and innate defenses. The