54. 35delG mutation in the connexin 26 gene is an autosomal recessive condition that has been identified to cause congenital deafness. In a population of 367 Greek children, 75 of the children carried two copies of the 35delG mutation. In order to calculate the percentage of individuals who are heterozygous for the 35delG mutation, the calculation that must be performed is Select one: a. 1 – (p2 – 2pq) b. 1 – (p +q) c. 1 – (p2 + q2) d. 1 – q2

54. 35delG mutation in the connexin 26 gene is an autosomal recessive condition that has been identified to cause congenital deafness. In a population of 367 Greek children, 75 of the children carried two copies of the 35delG mutation. In order to calculate the percentage of individuals who are heterozygous for the 35delG mutation, the calculation that must be performed is Select one: a. 1 – (p2 – 2pq) b. 1 – (p +q) c. 1 – (p2 + q2) d. 1 – q2

Name: 54.35delG mutation in the connexin 26 gene is an autosomal recessive c
Uploaded: 2024-03-20T06:42:55.000Z
Channel: Bartleby
Description: 54.35delG mutation in the connexin 26 gene is an autosomal recessive condition that has been identified to cause congenital deafness. In a population of 367 Greek children, 75 of the children carried two copies of the 35delG mutation.In order to calc

Curren'S Math For Meds: Dosages & Sol

11th Edition

ISBN:9781305143531

Author:CURREN

Publisher:CURREN

Chapter5: Unit, Percentage, Milliequivalent, Ratio, And Household Measures

Section: Chapter Questions

Problem 2.6P

See similar textbooks

Similar questions

152 Phenylketonuria (PKU) is a disorder caused by a recessive allele. Two carrier individuals have progeny. Answer the following questions in order and show solutions whenever relevant. If they have a normal child, what is the probability that he or she will be heterozygous? If they have three children, what is the probability of having 2 affected children and one normal child?
Tay–Sachs disease is caused by loss-of-function mutations ina gene on chromosome 15 that encodes a lysosomal enzyme.Tay–Sachs is inherited as an autosomal recessive condition.Among Ashkenazi Jews of Central European ancestry, about1 in 3600 children is born with the disease. What fraction ofthe individuals in this population are carriers?
A rare blinding disease that has a relation to dengenerative factors is partially penetrant. In the following pedigrees for two families, the affected symptomatic individuals (black circles and squares) have been diagnosed with this disease due to the mutation in mitochondrial DNA m.14484T>C. If III.4 is homoplasmic for m.14484T>C in hair, blood, urine and other tissues examined. What will occur with IV.7 then?
A woman with normal parents whose brother has phenylketonuria (PKU) marries a normal man who has a sister affected by PKU. If in a general population the incidence of PKU at birth is 1 in 3,600, what is the probability that their first child will be affected? 0.0017 0.0625 0.111 0.0033 0.998
Which of the following experimental observations suggest that adisease has a genetic basis?A. The frequency of the disease is less likely in relatives that liveapart compared with relatives that live together.B. The frequency of the disease is unusually high in a small groupof genetically related individuals who live in southern Spain.C. The disease symptoms usually begin around the age of 40.D. It is more likely that both monozygotic twins will be affectedby the disease than will dizygotic twins.
Why is the davson Danielli model wrong?
Suppose you use the semi-global Needleman-Wunsch algorithm to alignGAGATAGwithGACwhere match = 1, nonmatch = 0, gap = -1 When you do the backtracking, how many optimal paths will be found?
Which one of these is correct ? And why are the rest incorrect?
Six months pregnant, an expectant mother had a routineultrasound that showed that the limbs of the fetus wereunusually short. Her physician suspected that the babymight have a genetic form of dwarfism called achondroplasia,an autosomal dominant trait occurring with a frequency of about1 in 27,000 births. The parents were directed to a genetic counselorto discuss this diagnosis. In the conference, they learnedthat achondroplasia is caused by a mutant allele. Sometimes itis passed from one generation to another, but in 80 percent ofall cases it is the result of a spontaneous mutation that arisesin a gamete of one of the parents. They also learned that mostchildren with achondroplasia have normal intelligence and a normallife span. What information would be most relevant to concluding whichof the two mutation origins, inherited or new, most likelypertains in this case? How does this conclusion impact on thiscouple’s decision to have more children?
Six months pregnant, an expectant mother had a routineultrasound that showed that the limbs of the fetus wereunusually short. Her physician suspected that the babymight have a genetic form of dwarfism called achondroplasia,an autosomal dominant trait occurring with a frequency of about1 in 27,000 births. The parents were directed to a genetic counselorto discuss this diagnosis. In the conference, they learnedthat achondroplasia is caused by a mutant allele. Sometimes itis passed from one generation to another, but in 80 percent ofall cases it is the result of a spontaneous mutation that arisesin a gamete of one of the parents. They also learned that mostchildren with achondroplasia have normal intelligence and a normallife span. It has been suggested that prenatal genetic testing for achondroplasiabe made available and offered to all women. Wouldyou agree with this initiative? What ethical considerationswould you consider when evaluating the medical and societalconsequences of offering…
Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense mutation in the structural gene that encodes Lribulokinase, an enzyme that allows the bacteria to metabolize the sugar arabinose (R. Bost and R. Cribbs. 1969. Genetics 62:1–8). From the araB14 strain, they isolated some bacteria that possessed mutations that caused them to revert back to the wild type. Genetic analysis of these revertants showed that they possessed two different suppressor mutations. One suppressor mutation (R1) was linked to the original mutation in L-ribulokinase and probably occurred at the same locus. By itself, this mutation allowed the production of L-ribulokinase, but the enzyme produced was not as effective in metabolizing arabinose as the enzyme encoded by the wild-type allele. The second suppressor mutation (SuB) was not linked to the original mutation. In conjunction with the R1 mutation, SuB allowed the production of L-ribulokinase, but SuB by itself was not able…
Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense mutation in the structural gene that encodes Lribulokinase, an enzyme that allows the bacteria to metabolize the sugar arabinose (R. Bost and R. Cribbs. 1969. Genetics 62:1–8). From the araB14 strain, they isolated some bacteria that possessed mutations that caused them to revert back to the wild type. Genetic analysis of these revertants showed that they possessed two different suppressor mutations. One suppressor mutation (R1) was linked to the original mutation in L-ribulokinase and probably occurred at the same locus. By itself, this mutation allowed the production of L-ribulokinase, but the enzyme produced was not as effective in metabolizing arabinose as the enzyme encoded by the wild-type allele. The second suppressor mutation (SuB) was not linked to the original mutation. In conjunction with the R1 mutation, SuB allowed the production of L-ribulokinase, but SuB by itself was not able…