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Example research essay topic: Cystic Fibrosis Endoplasmic Reticulum - 717 words

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Cystic Fibrosis Commonly found in young children, Cystic Fibrosis is an inherited disease that is caused by a genetic disorder. The disease originates in the production of a critical protein that transports chloride ions from one place to another called a cystic fibrosis transmembrane conductance regulator (CFTR). The DNA of an infected person is missing three building blocks called nucleotides causing the CFTR protein to be missing one amino acid called phenylalanine. Normally, a healthy CFTR protein would be synthesized and then moved through the endoplasmic reticulum and golgi apparatus to pick up sugars before being released to the cell membrane. However, a defective CFTR protein does not leave the endoplasmic reticulum and is tagged for degradation. Other times the defective CFTR gene does not allow the protein to be created.

Whether or not the CFTR protein is produced, the diseased person does not get the CFTR protein needed to transport chloride ions. As a result, a number of symptoms and ultimately death occur. At first, an increase in salinity occurs in the sweat because the channels in the sweat glands do not remove chloride, a component of salt. The lack of chloride channels also affects important organs, such as the pancreas, liver, and the small intestine. The pancreas loses its ability to deliver digestive enzymes to certain areas of the body while the liver s bile ducts are clogged causing the liver to lose some of its function. Similarly, the small intestine is clogged by thick mucus.

Furthermore, cystic fibrosis causes infertility in men and some women by having the vas deferens blocked or the uterus blocked from sperm, respectively. The last symptom is tragically the most fatal. The air passages in the lungs become clogged with thick mucus causing the diseased person to die from lung cancer. Normally, the airway is lined with chloride and sodium channels that move chloride ions in and sodium ions out. This process ensures that the mucus remains in a liquid form and loose. The thin liquid nature of the mucus traps inhaled particles and allows the cilia lining the air passage the push the mucus up to the throat for removal.

However, in cystic fibrosis afflicted people, the missing chloride channel prevents the addition of chloride ions. In turn, the sodium uptake is enhanced causing the mucus in the passage to become thick and hard to remove. Furthermore, viruses and bacteria find their way into the clogged air passage attracting immune cells. Eventually, the bacteria infect and begin the deterioration of the passage. As a result, tissues and ultimately the lung itself become clogged and damaged causing death. At this time, treatments for cystic fibrosis are crude and do not ensure that the patient will live past his or her early adulthood.

For the affected organs, like the pancreas, scientists have developed a drug that will unclog the blocked passageways, so that the enzymes and other essential substances can flow to where they are needed. Antibiotics and anti-inflammatory drugs are being used to control bacterial infections and inflammations caused by immune system cells. Treatment for clogged air passageways remains quite medieval. Chest percussion, pounding on the chest to dislodge and expel the mucus, is common practice. In addition, a drug called DNase is used to liquefy and clear the mucus.

A healthy lung transplant can only replace the damaged lung. However, the future of cystic fibrosis treatment is quite bright. Besides premature screening of the parent-to-be, scientists are trying to develop a method that would prevent cystic fibrosis before it starts. Gene therapy, the placement of correct nucleotides in the DNA, would ensure that a person s body would synthesize correctly functioning proteins to channel chloride ions because the DNA has the blueprints for the protein. Furthermore, they have brought up the concept of putting healthy CFTR proteins into the cell. To counteract the CFTR proteins not being delivered to the cell membrane, scientists have proposed types of drugs that could either physically move the CFTR proteins from the endoplasmic reticulum to the cell membrane or cause other protein channels to increase chloride movement.

However, until this platform is achieved, doctors and scientists alike must continue to experiment and research until a cure is found. Bibliography Smith, Michael J. and Alan E. Smith, Cystic Fibrosis, Scientific American, Dec. 1995.


Free research essays on topics related to: small intestine, cystic fibrosis, endoplasmic reticulum, chloride, cell membrane

Research essay sample on Cystic Fibrosis Endoplasmic Reticulum

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