The major phenotype of deficiency of protolithic enzyme alpha-antitrypsin is the destruction of pulmonary alveoli resulting in chronic obstructive pulmonary disease or emphysema. The gene for this enzyme is highly polymorphic, with more than 70 different alleles described. 90% of white Europeans have MM genotype (normal). Two mutant alleles, S and Z, account for most of the disease associated with alpha-antitrypsin deficiency. The flowing table tabulates frequencies of different clinically important genotypes in the French population. Genotype Frequency MM 0.90 MZ 0.04 SS 0.001 SZ 0.0012 ZZ 0.0004 Using the data presented, calculate the allele frequencies for Z and S.

The major phenotype of deficiency of protolithic enzyme alpha-antitrypsin is the destruction of pulmonary alveoli resulting in chronic obstructive pulmonary disease or emphysema. The gene for this enzyme is highly polymorphic, with more than 70 different alleles described. 90% of white Europeans have MM genotype (normal). Two mutant alleles, S and Z, account for most of the disease associated with alpha-antitrypsin deficiency. The flowing table tabulates frequencies of different clinically important genotypes in the French population. Genotype Frequency MM 0.90 MZ 0.04 SS 0.001 SZ 0.0012 ZZ 0.0004 Using the data presented, calculate the allele frequencies for Z and S.

Curren'S Math For Meds: Dosages & Sol

11th Edition

ISBN:9781305143531

Author:CURREN

Publisher:CURREN

Chapter9: Parenteral Medication Labels And Dosage Calculation

Section: Chapter Questions

Problem 2.2P

See similar textbooks

Similar questions

Sickle-cell anemia is an interesting genetic disease. Normal homozygous individials (SS) have normal blood cells that are easily infected with the malarial parasite. Thus, many of these individuals become very ill from the parasite and many die. Individuals homozygous for the sickle-cell trait (ss) have red blood cells that readily collapse when deoxygenated. Although malaria cannot grow in these red blood cells, individuals often die because of the genetic defect. However, individuals with the heterozygous condition (Ss) have some sickling of red blood cells, but generally not enough to cause mortality. In addition, malaria cannot survive well within these "partially defective" red blood cells. Thus, heterozygotes tend to survive better than either of the homozygous conditions. 11% of an African population is born with a severe form of sickle-cell anemia (ss), What percentage of the population will be more resistant to malaria because they are heterozygous (Ss) for the sickle-cell…
Sickle-cell anemia is an interesting genetic disease. Normal homozygous individials (SS) have normal blood cells that are easily infected with the malarial parasite. Thus, many of these individuals become very ill from the parasite and many die. Individuals homozygous for the sickle-cell trait (ss) have red blood cells that readily collapse when deoxygenated. Although malaria cannot grow in these red blood cells, individuals often die because of the genetic defect. However, individuals with the heterozygous condition (Ss) have some sickling of red blood cells, but generally not enough to cause mortality. In addition, malaria cannot survive well within these "partially defective" red blood cells. Thus, heterozygotes tend to survive better than either of the homozygous conditions. 11% of an African population is born with a severe form of sickle-cell anemia (ss), What is the frequency of the dominant allele? Please show your work in order to receive credit.
Sickle-cell anemia is an interesting genetic disease. Normal homozygous individials (SS) have normal blood cells that are easily infected with the malarial parasite. Thus, many of these individuals become very ill from the parasite and many die. Individuals homozygous for the sickle-cell trait (ss) have red blood cells that readily collapse when deoxygenated. Although malaria cannot grow in these red blood cells, individuals often die because of this genetic defect causes deformation of red blood cells. However, individuals with the heterozygous condition (Ss) have some sickling of red blood cells, but generally not enough to cause mortality. In addition, malaria cannot survive well within these "partially defective" red blood cells. Thus, heterozygotes tend to survive better than either of the homozygous conditions. Assuming HWE, if 9% of an African population is born with a severe form of sickle-cell anemia (ss), what percentage of the population will be more resistant to malaria…
Sickle-cell anemia is an interesting genetic disease. Normal homozygous individials (SS) have normal blood cells that are easily infected with the malarial parasite. Thus, many of these individuals become very ill from the parasite and many die. Individuals homozygous for the sickle-cell trait (ss) have red blood cells that readily collapse when deoxygenated. Although malaria cannot grow in these red blood cells, individuals often die because of the genetic defect. However, individuals with the heterozygous condition (Ss) have some sickling of red blood cells, but generally not enough to cause mortality. In addition, malaria cannot survive well within these "partially defective" red blood cells. Thus, heterozygotes tend to survive better than either of the homozygous conditions. 11% of an African population is born with a severe form of sickle-cell anemia (ss), What is the frequency of the recessive allele? Please show your work in order
In a region of Africa, where malaria is prevalent, 40% of the population are found to have sickle-cell anemia. The disease is caused by an abnormal hemoglobin that is found in both homozygotes (S2S2) and heterozygotes (S1S2). Many homozygotes (S2S2) suffer from anemia and often die. Heterozygotes (S1S2) incur a much less debilitating malady called "sickling trait". Approximately 3% of the people with abnormal hemoglobin are homozygotes (1.2\% of the entire population). The fitness of the S2S2 homozygotes is only 1/4 that of the heterozygotes. Where malaria is prevalent, heterozygotes exhibit overdominance with respect to fitness. How would you calculate relative fitness of the S1S1 homozygotes if you're assuming the population is at an equilibrium frequency for S2?
As seen in Figure 24.20, freshwater water fleas (Daphnia) develop without hemoglobin (Hb) and are whitish when living in well-aerated water but produce abundant Hb and are red in O2- depleted water. Explain how each of these phenotypes could be advantageous (relative to the other) in the environment where it is expressed.
We often speak of diseases such as phenylketonuria (PKU) andachondroplasia as having a genetic basis. Explain whether the followingstatements are accurate with regard to the genetic basis ofany human disease (not just PKU and achondroplasia).A. An individual must inherit two copies of a mutant allele to havedisease symptoms.B. A genetic predisposition means that an individual has inheritedone or more alleles that make it more likely that she or he willdevelop disease symptoms than other individuals in a populationwill.C. A genetic predisposition to develop a disease may be passedfrom parents to offspring.D. The genetic basis for a disease is always more important thanthe environment.
Some people have a genetic predisposition for developing priondiseases. Examples are described in Table 25.6. In the case ofGerstmann-Straüssler-Scheinker disease, the age of onset istypically 30–50 years, and the duration of the disease (whichleads to death) is about 5 years. Suggest a possible explanationwhy someone can live for a relatively long time withoutsymptoms and then succumb to the disease in a relativelyshort time.
BACKGROUND Sickle cell disease is caused by a change in the gene for hemoglobin, which is the oxygen-carrying protein in red blood cells. Individuals who are homozygous for the sickle cell trait often cannot endure exercise. Individuals who are heterozygous for the trait can have sickle cell attacks under extreme conditions. Normal individuals (Hb Hb) have only normal hemoglobin. Homozygous sickle cell individuals (Hb Hb') have only sickle cell hemoglobin. Heterozygous individuals (Hbs Hb) have both normal hemoglobin and sickle cell hemoglobin. Jerry Smith collapsed while running a race for his track team. A doctor said that he had a sickle cell attack. Genetic tests were run on several family members. The test results are shown below. An X indicates that form of hemoglobin in red blood cells. PROBLEM How can you determine the genotypes of people in a family? TABLE 1. FAMILY PHENOTYPES Normal Hemoglobin Subject Jerry Smith Jerry's brother Jerry's younger sister Jerry's youngest sister…
One of the treatments for sickle cell anemia is hydroxyurea, which is known to induce the expression and production of fetal hemoglobin through a poorly defined mechanism. Explain how the increased expression of fetal hemoglobin can be a useful treatment for sickle cell anemia.
Given below is the electrophoretic profile of 2 proteins, a normal hemoglobin, HbA and the fetal hemoglobin, HbF. What information can be obtained from the profile shown? wwwwwww (+) HbF ww w (-) HbA ww ww A. HbF has a slightly different conformation compared with HbA B. HbF and HbA have different primary structures C. HbF has a higher affinity for oxygen than HbA D. HbF has a nonpolar amino acid residue in place of a basic amino acid. E. HbF has an acidic amino acid residue in place of a nonpolar amino acid
. Mutations in an autosomal gene in humans cause aform of hemophilia called von Willebrand disease(vWD). This gene specifies a blood plasma proteincleverly called von Willebrand factor (vWF). vWFstabilizes factor VIII, a blood plasma protein specified by the wild-type hemophilia A gene. Factor VIIIis needed to form blood clots. Thus, factor VIII is rapidly destroyed in the absence of vWF.Which of the following might successfully be employed in the treatment of bleeding episodes in hemophiliac patients? Would the treatments workimmediately or only after some delay needed forprotein synthesis? Would the treatments have only ashort-term or a prolonged effect? Assume that allmutations are null (that is, the mutations result in thecomplete absence of the protein encoded by the gene)and that the plasma is cell-free.a. transfusion of plasma from normal blood into avWD patientb. transfusion of plasma from a vWD patient into adifferent vWD patientc. transfusion of plasma from a hemophilia A…