Assignment Goals
Source Material
Student Instructions
Guiding Questions
Writing Prompt
Calibrations, Average Word Count, and Answer Keys

Assignment Goals

The objective for this CPR assignment is to integrate several different concepts addressed in your Human Physiology course to explain how a variety of different family genetic traits can lead to one single problem - heart failure (Silverthorn, p. 447-448).

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Source Material

This problem can be addressed using ONLY the knowledge presented in the Silverthorn textbook, if you can relate that knowledge to the gene defects that have been identified in families with high risk of heart failure. This assignment provides links to primary research abstracts in case you have questions about the links between heart failure and specific genes.

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Source Material Resources: Na,K-ATPase - The alpha1 Na,K-ATPase gene is a susceptibility hypertension gene in the Dahl salt-sensitiveHSD rat. J Clin Invest 1998 Sep 15;102(6):1102-11 URL: http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=9739044&form=6&db=m&Dopt=b beta-adrenergic receptor density - Beta-adrenergic receptor density and function in left ventricular hypertrophy in young essential hypertensives. J Hum Hypertens 2000 Jan;14(1):17-21 URL: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10673726&dopt=Abstract tropomyosin - Effects of two familial hypertrophic cardiomyopathy-causing mutations on alpha-tropomyosin structure and function. Biochemistry. 1999 Mar 23;38(12):3850. URL: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10090775&dopt=Abstract Hearts and Hypertension - A general resource on genetic links to heart diseases that includes an on-line video. URL: http://www.hhmi.org/grants/lectures/98lect/references.htm Troponin T - Altered regulatory function of two familial hypertrophic cardiomyopathy troponin T mutants. Biochemistry. 1999 Oct 5;38(40):13296-301. URL: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10529204&dopt=Abstract myosin heavy chain - Familial hypertrophic cardiomyopathy and atrial fibrillation caused by Arg663His beta-cardiac myosin heavy chain mutation. Am J Cardiol. 1999 Jun 17;83(12A):13H-18H. URL: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10750581&dopt=Abstract voltage-gated potassium channel - Missense mutation in the pore region of HERG causes familial long QT syndrome. URL: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8635257&dopt=Abstract epithelial sodium channel - Dysfunction of epithelial sodium transport: from human to mouse. Kidney Int. 2000 Apr;57(4):1313-8. URL: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10760060&dopt=Abstract aldosterone - [High prevalence of undiagnosed primary hyperaldosteronism among patients with essential hypertension]. Rev Med Chil 1999 Jul;127(7):800-6. URL: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10668287&dopt=Abstract actin - Alpha-cardiac actin is a novel disease gene in familial hypertrophic cardiomyopathy. J Clin Invest 1999 May 15;103(10):R39-43. URL: http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=10330430&form=6&db=m&Dopt=b

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Student Instructions

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Guiding Questions

Address the following points in your answer:

• List those genes whose function is required for muscle function and describe the role muscle function plays in congestive heart failure (Silverthorn, p. 447-448)?
• Describe the function of any of these genes that would alter responses of excitable cells such as contractile vascular and heart cells or the neurons required for most stimulus/response systems.
• Determine which genes play a role in kidney function for regulation of blood volume and explain how that would alter blood pressure and the workload for the heart.
• Support, verify, and justify your interpretation by including references to the abstracts or the Silverthorn text.
• Recommend treatments and/or future research that you would be willing to support with your tax dollars to improve the value and quality of life for families with these defects.

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  Writing Prompt

  At what age will you die? What do you need to know about the traits in your family to make decisions that will lead to a long, quality life? Listed here are nine hereditary trait variants that, when defective, have been linked to a genetic risk of heart failure in some families. Is there a high risk of heart failure in your family and, if so, how should that condition be treated? The mechanism for the hereditary cause may be an important factor in deciding how to treat heart disease.

  Review functions of each of these molecules. Discuss how defective protein function might lead to heart failure in each case. Your job will be easier if you group together traits with similar functional consequences.

  • Na,K-ATPase
  • beta-adrenergic receptor
  • tropomyosin
  • Troponin T
  • myosin heavy chain
  • voltage-gated potassium channel
  • epithelial sodium channel
  • aldosterone
  • actin

  Write in paragraph form your interpretation of how these defective traits contribute to heart failure. Support and justify each interpretation using citations from Silverthorn or the resource abstracts. Address each guiding question in your answer. Then recommend treatments and/or future research that you would be willing to support with your tax dollars to improve the value and quality of life for families with these defects.

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  Calibrations and Answer Keys

  
  Average Calibration Word Count = 346

  High Quality Calibration When we studied muscle, we learned how actin, myosin, troponin and tropomyosin worked together. In congestive heart failure, the regulation of contraction remains the same, but the heart muscle hypertrophies as the muscle fibers enlarge. This probably occurs as a result of the genes for each of the fibers being turned on for longer periods of time than normal. Four muscle genes have been associated with congestive heart failure: tropomyosin, troponin T, myosin heavy chain, and actin protein genes. Some of the genes related with congestive heart failure play a role in kidney function, such as genes encoding epithelial sodium channel (ENaC). According to Bonny and Hummler, ENaC is involved in sodium reabsorption in the distal nephron and regulates blood pressure. Mutations in ENaC cause hypertension from hyperfunction of sodium channels (Kidney Int, 2000). Hyperaldosteronism (high levels of aldosterone) is another trait related with hypertension that reduces sodium exctretion, resulting in increased blood pressure and increased heart workload (Rev Med. Chil, 1999). This happens because high levels of aldosterone increase sodium reabsorption. An increase in sodium reabsorption will cause water retention and increased fluid volume, leading to increased blood pressure. As blood pressure increases, the heart has to work harder to pump the blood, resulting in congestive heart failure. Another set of genes associated with hypertension is required for depolarization of excitable cells. Na, K-ATPase moves Na+ out and K+ into the cell (against their concentration gradients). Researchers have found a defective gene called the alpha 1 Na, K-ATPase gene that causes hypertension (J Clin Invest, 1998). A gene for the voltage-gated potassium channel also plays a role during cell membrane potential depolarization and repolarization. Both of these genes would interfere with signals in excitable cells like heart or nerve cells. Hypertension is a common risk factor for heart failure (Silverthorn, p. 448). I would put tax dollars towards blood pressure medication. Hopefully, this would ensure that everyone with hypertension would get treatment for it, to reduce the number of people who develop congestive heart failure.

  1. Does this text list all four muscle genes (tropomyosin, troponin T, myosin heavy chain, and actin) and state that these are required for muscle function?

  Yes No

  Answer: Yes

  Feedback : When we studied muscle, we learned how actin, myosin, troponin and tropomyosin worked together. In congestive heart failure, the regulation of contraction remains the same, but the heart muscle hypertrophies as the muscle fibers enlarge. This probably occurs as a result of the genes for each of the fibers being turned on for longer periods of time than normal. Four muscle genes have been associated with congestive heart failure: tropomyosin, troponin T, myosin heavy chain, and actin protein genes.

  2. Does the text state that the Na, K -ATPase gene is required for the functioning of excitable cells such as contractile vascular and heart cells or neurons?

  Yes No

  Answer: Yes

  Feedback : Another set of genes associated with hypertension is required for depolarization of excitable cells. Na, K-ATPase moves Na+ out and K+ into the cell (against their concentration gradients). Researchers have found a defective gene called the alpha 1 Na, K-ATPase gene that causes hypertension (J Clin Invest, 1998). A gene for the voltage-gated potassium channel also plays a role during cell membrane potential depolarization and repolarization. Both of these genes would interfere with signals in excitable cells like heart or nerve cells.

  3. The epithelial sodium channel plays an important role in sodium handling by the kidney, but NOT in excitable cells. Does this text relate the role of the epithelial sodium channel to the kidney?

  Yes No

  Answer: Yes

  Feedback : Some of the genes related with congestive heart failure play a role in kidney function, such as genes encoding epithelial sodium channel (ENaC). According to Bonny and Hummler, ENaC is involved in sodium reabsorption in the distal nephron and regulates blood pressure. Mutations in ENaC cause hypertension from hyperfunction of sodium channels (Kidney Int, 2000). Hyperaldosteronism (high levels of aldosterone) is another trait related with hypertension that reduces sodium exctretion, resulting in increased blood pressure and increased heart workload (Rev Med. Chil, 1999). This happens because high levels of aldosterone increase sodium reabsorption. An increase in sodium reabsorption will cause water retention and increased fluid volume, leading to increased blood pressure. As blood pressure increases, the heart has to work harder to pump the blood, resulting in congestive heart failure.

  4. Aldosterone controls sodium excretion and plays a key role in blood volume homeostasis. Does this author describe this function for aldosterone?

  Yes No

  Answer: Yes

  Feedback : Some of the genes related with congestive heart failure play a role in kidney function, such as genes encoding epithelial sodium channel (ENaC). According to Bonny and Hummler, ENaC is involved in sodium reabsorption in the distal nephron and regulates blood pressure. Mutations in ENaC cause hypertension from hyperfunction of sodium channels (Kidney Int, 2000). Hyperaldosteronism (high levels of aldosterone) is another trait related with hypertension that reduces sodium exctretion, resulting in increased blood pressure and increased heart workload (Rev Med. Chil, 1999). This happens because high levels of aldosterone increase sodium reabsorption. An increase in sodium reabsorption will cause water retention and increased fluid volume, leading to increased blood pressure. As blood pressure increases, the heart has to work harder to pump the blood, resulting in congestive heart failure.

  5. Does the text recommend treatments and/or future research based on the molecular physiology of heart or blood vessels?

  Yes No

  Answer: Yes

  Feedback : Hypertension is a common risk factor for heart failure (Silverthorn, p. 448). I would put tax dollars towards blood pressure medication. Hopefully, this would ensure that everyone with hypertension would get treatment for it, to reduce the number of people who develop congestive heart failure.

  6. Does this author support, verify, and justify their interpretation by including references to the abstracts or the Silverthorn text?

  Yes No

  Answer: Yes

  Feedback : Hypertension is a common risk factor for heart failure (Silverthorn, p. 448). I would put tax dollars towards blood pressure medication. Hopefully, this would ensure that everyone with hypertension would get treatment for it, to reduce the number of people who develop congestive heart failure.

  7. Does the essay have mechanical errors (that is, mistakes in spelling, grammar, and punctuation)?

  None Some (1 or 2) Many (more than 2)

  Answer: None

  Feedback : none

  8. Is the text coherent and integrated?

  Yes No

  Answer: Yes

  Feedback : none

  9. Does this essay waste words by discussing items that might be considered irrelevant material?

  Yes No

  Answer: No

  Feedback : none

  10. How would you rate this text?

  10 Highest 9 8 7 6 5 4 3 2 1 Lowest

  Rating: 9

  Feedback : none

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  Mid Quality Calibration Congestive heart failure is a leading cause of death in the United States today. Scientists and researchers still have not completely examined the causes of this disease. Congestive heart failure begins when hard work by the heart muscle causes the muscle fibers due to grow larger and stronger. This happens due to increased resistance to blood flow and the heart muscle is not able to handle the overloaded pressure and it begins to fail. Next, the left ventricle loses cardiac output while the right ventricle maintains its normal cardiac output. This action increases sympathetic signals to the ventricles to make the heart pump stronger and harder, but the heart cannot keep up with the increased resistance in response to sympathetic activity. Fluid builds up within the lungs and edema occurs. The edema interferes with oxygen exchange that will enable aerobic activity to occur and this lack of oxygen weakens the pumping of the heart even more, causing congestive heart failure. Mutations in the genes encoding human muscle proteins are related with congestive heart failure. Cardiac Troponin T mutations can cause familial hypertrophic cardiomyopathy, a disease that is characterized by ventricular hypertrophy and sudden premature death. Troponin T is the tropomyosin-binding subunit required for thin filament regulation of contraction. More than 40 different mutations have been identified in cardiac myosin heavy chain, another muscle protein, and these mutations also cause familial hypertrophic cardiomyopathy. Some individuals from these families have clinical manifestations such as increased incidence of sudden death. Reduced beta 2-adrenoreceptor function has also been linked to hypertensive people according to Calls et al, and NE signals through beta 2-adrenoreceptor to increase pumping by the heart, so not all of the genetic defects leading to congestive heart failure occur in muscle proteins. By learning how to screen for genetic mutations and defects, preventive measures can be taken so that those suffering from certain life threatening hereditary traits can be treated before it is too late.

  1. Does this text list all four muscle genes (tropomyosin, troponin T, myosin heavy chain, and actin) and state that these are required for muscle function?

  Yes No

  Answer: No

  Feedback : Mutations in the genes encoding human muscle proteins are related with congestive heart failure. Cardiac Troponin T mutations can cause familial hypertrophic cardiomyopathy, a disease that is characterized by ventricular hypertrophy and sudden premature death. Troponin T is the tropomyosin-binding subunit required for thin filament regulation of contraction. More than 40 different mutations have been identified in cardiac myosin heavy chain, another muscle protein, and these mutations also cause familial hypertrophic cardiomyopathy. Some individuals from these families have clinical manifestations such as increased incidence of sudden death. Reduced beta 2-adrenoreceptor function has also been linked to hypertensive people according to Calls et al, and NE signals through beta 2-adrenoreceptor to increase pumping by the heart, so not all of the genetic defects leading to congestive heart failure occur in muscle proteins.

  2. Does the text state that the Na, K -ATPase gene is required for the functioning of excitable cells such as contractile vascular and heart cells or neurons?

  Yes No

  Answer: No

  Feedback : none

  3. The epithelial sodium channel plays an important role in sodium handling by the kidney, but NOT in excitable cells. Does this text relate the role of the epithelial sodium channel to the kidney?

  Yes No

  Answer: No

  Feedback : none

  4. Aldosterone controls sodium excretion and plays a key role in blood volume homeostasis. Does this author describe this function for aldosterone?

  Yes No

  Answer: No

  Feedback : none

  5. Does the text recommend treatments and/or future research based on the molecular physiology of heart or blood vessels?

  Yes No

  Answer: Yes

  Feedback : By learning how to screen for genetic mutations and defects, preventive measures can be taken so that those suffering from certain life threatening hereditary traits can be treated before it is too late.

  6. Does this author support, verify, and justify their interpretation by including references to the abstracts or the Silverthorn text?

  Yes No

  Answer: Yes

  Feedback : Mutations in the genes encoding human muscle proteins are related with congestive heart failure. Cardiac Troponin T mutations can cause familial hypertrophic cardiomyopathy, a disease that is characterized by ventricular hypertrophy and sudden premature death. Troponin T is the tropomyosin-binding subunit required for thin filament regulation of contraction. More than 40 different mutations have been identified in cardiac myosin heavy chain, another muscle protein, and these mutations also cause familial hypertrophic cardiomyopathy. Some individuals from these families have clinical manifestations such as increased incidence of sudden death. Reduced beta 2-adrenoreceptor function has also been linked to hypertensive people according to Calls et al, and NE signals through beta 2-adrenoreceptor to increase pumping by the heart, so not all of the genetic defects leading to congestive heart failure occur in muscle proteins.

  7. Does the essay have mechanical errors (that is, mistakes in spelling, grammar, and punctuation)?

  None Some (1 or 2) Many (more than 2)

  Answer: None

  Feedback : none

  8. Is the text coherent and integrated?

  Yes No

  Answer: Yes

  Feedback : none

  9. Does this essay waste words by discussing items that might be considered irrelevant material?

  Yes No

  Answer: No

  Feedback : none

  10. How would you rate this text?

  10 Highest 9 8 7 6 5 4 3 2 1 Lowest

  Rating: 6

  Feedback : none

  Top
  

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  Low Quality Calibration One thing we know is that diseases of the heart and blood vessels are responsible for nearly half of all deaths in the US. Risk factors that cannot be controlled include gender, age, and family history of cardiovascular disease. Heredity also plays an important role. If a person has one or more family members with heart disease, their risk is elevated. Many genetic defects can contribute to heart failure. Mutated genes that alter kidney function can also affect the heart because an increase of sodium in the system will increase the risk of hypertension. The Na,K-ATPase gene is important in humans because it maintains the concentration gradients of sodium and potassium ions across each cell membrane. A study done on rats shows that a defective Na,K-ATPase gene in animals causes increased susceptibility to hypertension. Data on research done on Dahl salt sensitive and Dahl salt resistant rats showed that the Alpha 1 Na K-ATPase gene was a susceptibility gene for salt sensitive hypertension in the Dahl S rat model. Transgenic Dahl S rats exhibited less salt sensitive hypertension, less hypertensive renal disease and longer life span compared to the nontransgenic Dahl S rat controls. Rationale for reducing salt intake to control hypertension is that salt causes water retention. Blood pressure will increase if circulating blood volume increases. In most people, the kidney functions to get rid of excess sodium, but in those people who inherit a defective gene for sodium handling, it may be necessary to reduce salt intake in order to control the fluid volume and hence the blood pressure. By reducing salt in the diet, these people can decrease retention of fluid in the extracellular compartment. Gene research and gene therapy can lead to early detection for these people so that they can restrict their salt consumption and live as long as possible. Early detection also means that carriers can make informed decisions on whether or not they want to take a chance of passing these diseases on to their children. But in the case of people who get congestive heart failure due to a gene that is NOT related to kidney function, reduction of salt consumption may not work to control their blood pressure and prevent congestive heart failure.

  1. Does this text list all four muscle genes (tropomyosin, troponin T, myosin heavy chain, and actin) and state that these are required for muscle function?

  Yes No

  Answer: No

  Feedback : none

  2. Does the text state that the Na, K -ATPase gene is required for the functioning of excitable cells such as contractile vascular and heart cells or neurons?

  Yes No

  Answer: No

  Feedback : One thing we know is that diseases of the heart and blood vessels are responsible for nearly half of all deaths in the US. Risk factors that cannot be controlled include gender, age, and family history of cardiovascular disease. Heredity also plays an important role. If a person has one or more family members with heart disease, their risk is elevated. Many genetic defects can contribute to heart failure. Mutated genes that alter kidney function can also affect the heart because an increase of sodium in the system will increase the risk of hypertension. The Na,K-ATPase gene is important in humans because it maintains the concentration gradients of sodium and potassium ions across each cell membrane. A study done on rats shows that a defective Na,K-ATPase gene in animals causes increased susceptibility to hypertension. Data on research done on Dahl salt sensitive and Dahl salt resistant rats showed that the Alpha 1 Na K-ATPase gene was a susceptibility gene for salt sensitive hypertension in the Dahl S rat model. Transgenic Dahl S rats exhibited less salt sensitive hypertension, less hypertensive renal disease and longer life span compared to the nontransgenic Dahl S rat controls. Rationale for reducing salt intake to control hypertension is that salt causes water retention. Blood pressure will increase if circulating blood volume increases. In most people, the kidney functions to get rid of excess sodium, but in those people who inherit a defective gene for sodium handling, it may be necessary to reduce salt intake in order to control the fluid volume and hence the blood pressure. By reducing salt in the diet, these people can decrease retention of fluid in the extracellular compartment. Gene research and gene therapy can lead to early detection for these people so that they can restrict their salt consumption and live as long as possible. Early detection also means that carriers can make informed decisions on whether or not they want to take a chance of passing these diseases on to their children. But in the case of people who get congestive heart failure due to a gene that is NOT related to kidney function, reduction of salt consumption may not work to control their blood pressure and prevent congestive heart failure.

  3. The epithelial sodium channel plays an important role in sodium handling by the kidney, but NOT in excitable cells. Does this text relate the role of the epithelial sodium channel to the kidney?

  Yes No

  Answer: Yes

  Feedback : One thing we know is that diseases of the heart and blood vessels are responsible for nearly half of all deaths in the US. Risk factors that cannot be controlled include gender, age, and family history of cardiovascular disease. Heredity also plays an important role. If a person has one or more family members with heart disease, their risk is elevated. Many genetic defects can contribute to heart failure. Mutated genes that alter kidney function can also affect the heart because an increase of sodium in the system will increase the risk of hypertension. The Na,K-ATPase gene is important in humans because it maintains the concentration gradients of sodium and potassium ions across each cell membrane. A study done on rats shows that a defective Na,K-ATPase gene in animals causes increased susceptibility to hypertension. Data on research done on Dahl salt sensitive and Dahl salt resistant rats showed that the Alpha 1 Na K-ATPase gene was a susceptibility gene for salt sensitive hypertension in the Dahl S rat model. Transgenic Dahl S rats exhibited less salt sensitive hypertension, less hypertensive renal disease and longer life span compared to the nontransgenic Dahl S rat controls. Rationale for reducing salt intake to control hypertension is that salt causes water retention. Blood pressure will increase if circulating blood volume increases. In most people, the kidney functions to get rid of excess sodium, but in those people who inherit a defective gene for sodium handling, it may be necessary to reduce salt intake in order to control the fluid volume and hence the blood pressure. By reducing salt in the diet, these people can decrease retention of fluid in the extracellular compartment. Gene research and gene therapy can lead to early detection for these people so that they can restrict their salt consumption and live as long as possible. Early detection also means that carriers can make informed decisions on whether or not they want to take a chance of passing these diseases on to their children. But in the case of people who get congestive heart failure due to a gene that is NOT related to kidney function, reduction of salt consumption may not work to control their blood pressure and prevent congestive heart failure.

  4. Aldosterone controls sodium excretion and plays a key role in blood volume homeostasis. Does this author describe this function for aldosterone?

  Yes No

  Answer: No

  Feedback : none

  5. Does the text recommend treatments and/or future research based on the molecular physiology of heart or blood vessels?

  Yes No

  Answer: Yes

  Feedback : One thing we know is that diseases of the heart and blood vessels are responsible for nearly half of all deaths in the US. Risk factors that cannot be controlled include gender, age, and family history of cardiovascular disease. Heredity also plays an important role. If a person has one or more family members with heart disease, their risk is elevated. Many genetic defects can contribute to heart failure. Mutated genes that alter kidney function can also affect the heart because an increase of sodium in the system will increase the risk of hypertension. The Na,K-ATPase gene is important in humans because it maintains the concentration gradients of sodium and potassium ions across each cell membrane. A study done on rats shows that a defective Na,K-ATPase gene in animals causes increased susceptibility to hypertension. Data on research done on Dahl salt sensitive and Dahl salt resistant rats showed that the Alpha 1 Na K-ATPase gene was a susceptibility gene for salt sensitive hypertension in the Dahl S rat model. Transgenic Dahl S rats exhibited less salt sensitive hypertension, less hypertensive renal disease and longer life span compared to the nontransgenic Dahl S rat controls. Rationale for reducing salt intake to control hypertension is that salt causes water retention. Blood pressure will increase if circulating blood volume increases. In most people, the kidney functions to get rid of excess sodium, but in those people who inherit a defective gene for sodium handling, it may be necessary to reduce salt intake in order to control the fluid volume and hence the blood pressure. By reducing salt in the diet, these people can decrease retention of fluid in the extracellular compartment. Gene research and gene therapy can lead to early detection for these people so that they can restrict their salt consumption and live as long as possible. Early detection also means that carriers can make informed decisions on whether or not they want to take a chance of passing these diseases on to their children. But in the case of people who get congestive heart failure due to a gene that is NOT related to kidney function, reduction of salt consumption may not work to control their blood pressure and prevent congestive heart failure.

  6. Does this author support, verify, and justify their interpretation by including references to the abstracts or the Silverthorn text?

  Yes No

  Answer: No

  Feedback : none

  7. Does the essay have mechanical errors (that is, mistakes in spelling, grammar, and punctuation)?

  None Some (1 or 2) Many (more than 2)

  Answer: None

  Feedback : none

  8. Is the text coherent and integrated?

  Yes No

  Answer: Yes

  Feedback : none

  9. Does this essay waste words by discussing items that might be considered irrelevant material?

  Yes No

  Answer: No

  Feedback : none

  10. How would you rate this text?

  10 Highest 9 8 7 6 5 4 3 2 1 Lowest

  Rating: 4

  Feedback : none

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