CFTR Scavenger Hunt Instructions-

This scavenger hunt consists of half a dozen questions for you to hunt the internet for answers for. Each question has multiple answers so find as many as you can before proceeding. The next part consists of several questions that you are to answer without the use of outside resources. You should be able to answer these with the information you have gathered plus your own thinking. A list of possible answers and a list of learning objectives may be found at the end of this project.

Once you have understood these instructions jump to the next part by clicking here.

Scavenger hunt for these items using any resource-

1. What organs and tissues are CFTR proteins found in?
2. What diseases are CFTR proteins involved in?
3. What are some specific examples of deficient or absent CFTR activity?
4. What are some specific examples of excessive CFTR activity?
5. What signal transduction cascade steps are involved in regulation of CFTR in the intestine?
6. What are the disease mechanisms of cholera at the molecular level?

Once you have hunted down as many answers to each of these questions jump to the next part by clicking here.

Work out answers to these questions using no outside resources-

7. From the point of view of the Vibrio cholerae bacterium, though it is deadly to its host in a short time, what characteristics of the bacterium contribute to its survival?
8. From the point of view of the individual with cholera, what can be done to contribute to survival even without antibiotics?
9. From the point of view of public health, what can contribute to prevention of cholera?

Once you have developed as many answers to each of these questions view an answer key by clicking here.

Key:

1. lungs, pancreas, intestines, sweat glands, biliary tree, vas deferens, lower expression in others
2. cystic fibrosis, cholera, typhoid fever, congenital bilateral absence of the vas deferens and hereditary pancreatitis (certain CFTR mutations may lead to the latter two disorders separately than cystic fibrosis).
3. inability to clear certain bacteria from lung which after decades of resulting inflammation results in fibrotic lung (cystic fibrosis), increased viscosity pancreatic secretions causing deficiency of pancreatic digestive enzymes (cystic fibrosis and hereditary pancreatitis), inability to form functional vas deferens (cystic fibrosis and congenital bilateral absence of the vas deferens ), inability to reabsorb chloride and sodium from sweat resulting in increased salt content in sweat (cystic fibrosis- used as diagnostic technique), inability of certain bacteria that rely on CFTR for cell entry to enter the blood via intestinal cells (protection from typhoid fever)
   
4. secretion of intestinal fluid to the point of diarrhea and even death (cholera)
5. vasoactive intestinal peptide (ligand) is the signal, the steps involve binding to G protein coupled receptor, activation of a Gs protein, activation of adenylate cyclase, and activation of protein kinase A, which controls CFTR, and the physiological action is a regulated chloride ion conductance accompanied osmotically by water secretion into the gut
6. runaway upregulation of CFTR, VCC pore forming complex mediates additional conductance of Cl-, ZOT blocks assembly of tight junctions between intestinal epithelial cells
7. Vibrio cholerae reproduces in the intestine of one person, causes its own rapid expulsion and spread from that person into the environment, is unfortunately consumed by the next person, forming an efficient cycle
8. cholera is accompanied by massive dehydration which can be balanced by copious rehydration accompanied by electrolytes, at some point the immune system will stop the bacterial infection
9. the cycle referred to above whereby cholera is passed from one person to another can be broken by proper sanitation and food safety, this is easier in some parts of the world than in others

View the learning objectives for this scavenger hunt by clicking here.

Learning Objectives:

1. Apply biomedical informatics to gather complete information.
2. Examine diverse aspects of the CFTR protein.
3. Locate multiple functions of the CFTR protein.<
4. Characterize malfunctions of the CFTR protein.<
5. Propose reasons for the success of cholera to propagate.
6. Develop simple means by which a cholera infection may be treated.
7. Formulate steps by which the infection cycle of cholera may be broken.<

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