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Biochemistry

Obesity is polygenic disorder that results from a combination of many factors. When combined with lack of physical activity, obesity leads to a cluster of conditions that combined result in a disease state.

a) What is the name given to this combination of disorders?

b) List and briefly describe the 5 clinical criteria that are used in the diagnosis of this disease.

c) List 1 treatment method for this disorder.

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Collen Von
Collen VonLv2
28 Sep 2019
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Related questions

PLEASE ANSWER ALL QUESTIONS..PLEASE NOT ONLY 1 QUESTION. THANK YOU

QUESTION 1. Chronic diseases generally have several underlying characteristics, including a.A long latency period between exposure to risk and disease outcomes b. Low degree of preventability c. High curve rate d.None of the above

QUESTION 2.Which of the following risk factors collectively explain a significant proportion (not incidence) of most chronic diseases. a.Tobacco, alcohol, diet b.Tobacco, alcohol, diet, physical activity c. Alcohol, physical activity d.Tobacco, diet, physical activity

QUESTION 3.Adherence to treatment is influenced by several interacting dimensions including a.Social and economic factors b. Healthcare system factors c.Condition-related factors d.Therapy-related factors e.Patient related factors f.All of the above

QUESTION 4. _________ is the leading cause of cancer in both developed and developing countries worlwide a.Radiation exposure b. Tobacco use c.Pesticide exposure d.Air pollution

QUESTION 5.This week's YouTube video on treating non-communicable diseases in Rwanda showed how a community health worker helps to treat heart disease, diabetes and _______ a.Cancer b.Asthma c.Hepatitis d.HIV/AIDS

QUESTION 6.Which of these are myths of chronic disease control a.Benefits of chronic disease control accrue not only to the individual but also to the population b.Economic growth improves all health conditions c. Chronic diseases are associated with low SES/poverty d.Chronic disease only occurs in the elderly e.a and c f.b and d

QUESTION 7 ___________ remains the leading cause of death among both men and women in low- and middle-income countries a.Cancer b.Cardiovascular disease c. Diabetes d.Obesity e.Respiratory disease

QUESTION 8.Chronic disease in adults accounts for approximately 60% of all deaths worldwide. True False

QUESTION 9.The WHO's Innovative Care for Chronic Conditions Framework includes a positive policy environment. True False

QUESTION 10.It is estimated that the overall number of cancer cases will rise by 50% in the next 20 years. True False

QUESTION 11.Comorbidity refers to simultaneous occurrence in a person of two or more disorders; comorbid conditions can increase the risk of adverse outcomes. True False

QUESTION 12.Emerging evidence supports starting promotion efforts during pregnancy and early childhood and continuing efforts throughout life lower exposures to major chronic disease risk factors. True False

QUESTION 13. Increased cumulative exposure to risk factors over the lifecourse combined with social and economic inequalities, leads to the levels of inequalities seen in later adult life. True False

QUESTION 14.The "compression of morbidity" model proposes that morbidity due to aging cannot be postponed or mitigated by disease prevention programs True False

QUESTION 15.There is few significant funding sources for chronic diseases in low-and middle-income countries. True False

QUESTION 16.To combat chronic diseases, modern, evidence-based interventions emphasize shared decision making and collaborative goal setting among providers and patients. True False

QUESTION 17.In the absence of legislative, financial and engineering approaches, health education programs often have a limited impact on preventing or reducing chronic diseases. True False

QUESTION 18. It is estimated that deaths from diet-related chronic disease in China will triple between 1995 and 2025. True False

QUESTION 19.The third highest percent of global DALY's is attributed to which risk factor? a.Alcohol use b.Tobacco use c.Unsafe sex d.Childhood underweight

QUESTION 20.In the 1990's which country experienced a substantial decline in male life expectancy as a result of dramatic socio-political changes a.China b.Russia c. India d.Canada

INSTRUCTIONS

Go to the OMIM database on the NCI portal. Search for PAH, select the first record on the list The following page will appear: Read the initial information Phenylketonuria (PKU) is an autosomal recessive inborn error of metabolism resulting from a deficiency of the enzyme PAH (Phenylalanine Hydroxylase). Lack of PAH enzyme activity results in elevated level of phenylalanine. On the other hand, mutations in the PAH gene can also result in a milder disease called hyperphenylalaninemia (HPA) characterized by an elevated level of phenylalanine without the cognitive impairment associated with PKU. QUESTIONS

Question 1: Consider two actual DNA mutations found as 2 PAH mutant alleles. a. Mutation # 0017 changes codon 414 from a tyrosine to a cysteine (TYR414CYS). A homozygous genotype leads to HPA. Indicate the type of mutation for 0017 at the DNA level. Identify the class of mutation at the protein level. Based on the disease phenotype, would you expect the mutated protein to be partially functional or non-functional? (I think it is functional..? http://www.omim.org/entry/612349) Explain your reasoning briefly b. . Mutation #0018 is a mutation that changes the splice site of intron 4 (IVS4). Explain the consequence of mutation 0018 at the level of transcription of the gene, splicing and protein synthesis. Homozygous 0018 leads to PKU phenotype Question 3: Assume an individual heterozygote for 0017/0018. ?Which special term is used to describe a heterozygote with two different mutant alleles - Compound heterozygote Where along the dominance-recessivity scale would the phenotype of this individual falls in relation to the phenotype of the two mutant homozygotes? Explain briefly.

Cystic Fibrosis (CF) is an autosomal recessive genetic disease that is characterized by the secretion of thick, abnormal mucous in the lungs. The mutated gene that leads these symptoms is the CF transmembrane conductance regulator (CFTR gene). The encoded protein is a chloride channel that moves chloride ions out of epithelial cells. In a homozygous individual, the lack of this chloride channel function in a mutant slows the flow of water into extracellular spaces. This lack of water export leads to the heavy mucus in the lungs of CF patients. Although children with CF would die in childhood, current treatments provide life expectancies into the 30’s.

CF is the most frequently inherited genetic disorder among American children. It affects 1 of every 2,500 children; 30,000 currently have the disease. Although its frequency is higher in European populations, it affects all human populations. Heterozygous carrier frequencies in the US are estimated to be 1 out of 29 Caucasians, 1 out of 46 Hispanics, 1 out of 61 African Americans and 1 out of 90 Asians. There are genetic screens for carriers of CF but they are not routinely performed despite this high frequency of carriers. At least all states in the US proscribe testing of newborns to identify children with CF early so that treatment can be started. Newborn tests for CF: http://www.cff.org/AboutCF/Testing/NewbornScreening/ScreeningforCF/ . If CF is such a common genetic disease, and such a simple Mendelian trait, why is genetic screening of parents not done more frequently? Is it just economic, a pain to do, or is it more complex such that the results of genetic testing are not just positive or negative?

Answer the following questions:
1. If two parents are heterozygous carriers of CF, show a pedigree with four children showing the incidence of carriers and afflicted children. If each unafflicted child (carrier or not) mates with another person, who has a 1 out of 30 chance of being a carrier of CF, what is the expected incidence CF disease in the third generation (frequency of CF in any one of grandchildren of the original couple)?

2. Pleiotropy of Cystic Fibrosis. Watch the two videos on the left at:

http://www.cftrscience.com/MOD-animation
or, if you can not view these, read the short NIH Genetics Home Reference for Cystic Fibrosis http://ghr.nlm.nih.gov/condition/cystic-fibrosis

Connect the description with one of the following videos, or related ones (there are many) you see:
video (10 minutes) of daily life of a child with Cystic Fibrosis http://www.youtube.com/watch?v=WUsuGKzdDg8
Laura’s (20 year old) video diary of life with CF http://www.youtube.com/watch?v=Pgrf8qJXhpc&feature=related

In your own words, describe the range of CF phenotypes. List the other organs besides lungs that are affected and how does it affects those organs.

3.The DNA sequence of the CFTR gene is 170,000 base pairs in length and encodes the CFTR protein that is 1480 amino acids long. Open the accompanying text file (in Canvas/Files/Discussion folder) “CFTR gene DNA sequence”. You will see an alignment of the NIH human genome sequence of the CFTR gene – called “Reference” rather than “wild-type”- against a gene sequence containing a common mutation in CFTR. Look at the alignment and determine how the DNA sequence differs between them. What is the position number where they differ? How many and what nucleotides do they differ in? A “-“ mark in one sequence in the alignment means that that base sequence is missing the corresponding bases in the other sequence. The sequence is a long one but the differences are in bolded bright red text. Matching sequence is marked with a | linking the two sequences. Look near the sequence AAATATCATC if you use FIND tool in Word.

In another file, you will an alignment of the reference translated into a protein sequence, compared to the mutant allele translated into protein sequence. The differences are again in red whereas the areas where the proteins match are in black. Look at the alignment. How do these two proteins differ? Again, find the position number and describe how they differ at that location. A “-“ mark in the alignment means that amino acid is missing when compared to the other sequence.

4. Given that the CFTR gene can be analyzed for a mutation that causes CF, couples interested in being tested as carriers face several choices given the results.
What could be a consequence of a false positive result (couple is identified as carriers but they would not produce any children with symptoms)?

What could be a consequence of a false negative result (a test indicates the couple is not both carriers but they would produce some children with CF)?

5. The sensitivity of the test can vary with ethnic group. The following is a chart from the NCBI Genetic testing site. A sensitivity less than 100% would be likely to produce false negative results from an inability to determine that someone is carrier.

CF Carrier Test Sensitivity by Ethnic Group
http://www.ncbi.nlm.nih.gov/projects/GeneTests/static/concepts/primer/ptscarr5.shtml

Ethnic Group 1

Population Frequency of CF

Sensitivity of Carrier Detection 2

Caucasian

1 in 29

90%

Ashkenazi Jewish

1 in 29

97%

Native American

1 in 32

94%

Latino

1 in 46

57%

African-American

1 in 60

75%

Asian

1 in 90

30%

Why might different ethnic populations differ in the ability of the genetic test to identify carriers of CF?

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