Genetics of Sickle Cell Anemia

Sickle Cell Anemia is an inherited form of anemia, a condition in which there isn’t enough healthy red blood cells to carry sufficient oxygen throughout your body. Normally a person has flexible and round blood cells. With Sickle Cell anemia, Hemoglobin molecules in red blood cells, that carry oxygen in the body, are defective causing some of the red blood cells to change and form a sickle, or crescent moon shape.

In a large, randomly mating population where mutations, migration, and natural selection are no longer viable, the allele and genotypic frequencies will remain at equilibrium. If any of these conditions are changed, then the allele and genotype frequencies will be unable to maintain genetic equilibrium.

From the data we can conclude that different traits or parameters can effect a population in many different ways. It can decrease or increase a population depending on the trait. After a hurricane hits Lake Malawi the cichlid fish male population must adapt to the new factors that have been put upon them. Mutation within the population supports the fact that it can cause dominant and recessive allele frequency to decrease. Migration causes the allele frequency to lower as well due to movement of the population after the hurricane. The cichlid male fish with a higher fitness are more suitable for their environment, but when their fitness is lowered, their allele frequency decreases. This

Sickle-Cell Anemia is an inherited, chronic blood disease in which the body produces abnormally shaped red blood cells. When the blood cells become crescent/sickle shaped, they are unable to deliver adequate amounts of oxygen to other cells. Also, these unusual “sickle” cells block blood pathways to the limbs and organs, limiting the amount of blood flowing throughout the body. It causes pain, organ damage, and anemia (low blood count). Unfortunately, however, when sufferers are born with this disease, they live life knowing it is incurable.

The focal point of this journal article focused on how the inherited genetic disease; Sickle cell anemia, is influenced by ethnicity and ancestry; two key categories that must be considered when explaining genetic associations and comparing traits amongst a population. This article compared the genetic profiles of African Americans with sickle cell disease to individuals of the Caucasian/ European descent and African descent. They discovered that although there is slight genetic comparison between ethnicity, there are more similarity in relation to ancestry and the Sickle cell trait. Three ancestry’s that resonated the most were the Mandinka’s, Yoruba’s, and Bantu from West Africa. In this study, researchers combined genome data from different

For this experiment we assume that the organisms’ survival depends upon a single gene with two alleles, A & a, that show incomplete dominance. Furthermore, these alleles combine to form three genotypes: AA, Aa, & aa. All 3 genotypes are phenotypically expressed as varying traits of the organism as follows:

Sickle Cell Disease is a genetic disease caused by a SNP (Single Nucleotide Polymorphism). Which means it is caused by a single letter gene mutation. Through the advent of CRISPR/Cas9 the disease might be cured. It is a serious reality and will enter medical trials within a handful of years. Sickle Cell Disease is an inherited disease that predominantly affects people of African descent. Red Blood cells become rigid and sickle shaped, causing blockages and pain crises. In cases of Sickle Cell Disease the Beta-Globin are mutated causing faulty and deformed Hemoglobin proteins thus creating sickled and short-lived Red Blood Cells.

As for the homozygous ebony genotype (e/e), there was an increase by week three, followed by steep decrease on week five and seven. Unlike the homozygous genotype, the heterozygous (+/e) frequencies did not fluctuate as much. There was a pattern of a small decrease followed by increase over the course of seven weeks.

A genetic disorder caused by the abnormal gene for hemoglobin S is called sickle cell anemia. Only replace that take place in glutamic acid is to fill in for valine as the sixth codon of the hemoglobin protein, which alter declines the hemoglobin’s ability transform oxygen throughout your body. The human body needs oxygen in order to function when we eat food and liquid for energy even including muscles, repairs our cells, feeds our brain, breath and nerves. Normal cells are described as round, red, flexible and travel easily throughout your blood vessels. Sickle cell anemia describes a red blood cell that has inflexible, tacky, and create like a crescent moons not like the normal red cells. It tends to slow down or block the blood flows while

Sickle cell anaemia describes a hereditary autosomal recessive disorder that affects a protein found in red blood cells (erythrocytes) called haemoglobin. This disease results in 100% of blood cells becoming sickle shaped. The co-dominant sickle cell disease entails half of the erythrocytes becoming sickle shaped and the remaining half as normal biconvex structures, however, these people are carriers and can pass the disease or anaemia onto their offspring. Prevalence of significant morbidity and mortality of sickle cell disease is clear in Africa, the Mediterranean, India, Central America and the Carribean, with estimates suggesting 250 000 children are born annually with sickle cell anaemia (reference). Haemoglobin ss the autosomal recessive genotype, inherited from both parents, causes the phenotype of sickle cell anaemia. When erythrocytes become rigid and sticky, they cannot flow smoothly through small vessels, consequently, slowing or blocking blood flow and oxygen around the body. This prevents oxygen from reaching vital organs such as the spleen, liver, lugs, heart and kidneys, causing extensive damage as lack of oxygen results in cell death.(1) Sickle cells only live an

This paper looks in depth at the disease process of sickle cell anemia. It starts out by covering the pathophysiology of the disease and how it functions within the body. The second section of the paper covers the ways to manage sickle cell anemia, whether it be by medication or blood transfusions, or both. The third section is meant to emphasize the important assessment details and how things should be prioritized for the patient with this disease; it also defines which lab values are most important to monitor for the patient. The paper concludes with a case study which details an African American family wishing to start a family. They undergo genetic counseling and receive information on the impact of sickle cell anemia in regards to

(4) When a population changes (either increases or decreases) for seemingly no reason, genetic drift is most often to blame. (1) Frequencies of alleles available in the gene pool for that population are subject to change when evolution takes place, and one or more alleles can sometimes vanish. Populations with fewer organisms often experience more substantial genetic drift, due to the fact that if there is less of an allele in a gene pool during a generation, there is a higher risk that a large amount of that allele will be removed just due to random chance – genetic drift. (4) It is important to note that the final population during the “frequent disasters” trial became 243 from an original 4000 when one of the alleles (“a”) was lost. This is considered a “population bottleneck” (4) where the population decreased by a significant amount. In a situation like this, there are fewer alleles available in the gene pool of that population for that generation, so there is a bigger chance that genetic drift will accidently cause the loss of a substantial portion of one of the alleles, driving it to discontinuation.

The Effect of Natural Selection, Heterozygote Advantage, and Genetic Drift on the Allele Frequencies Over Time

Imagine living a life with misleading information about a younger sibling's death. Many wonder why God took them, but not myself. For the simple fact the morning of Madison’s passing God told me everything would be okay. Experiencing this at such young age makes thou think of the extreme; however, it makes thee stronger. The idea of this paper is to break down the information and show everyone how Sepsis breaks down the body. Along, with linking Sepsis with Sickle Cell Trait when the body is already weak and cannot fight off the infection.

Sickle Cell Trait (SCT) and Sickle Cell Disease (SCD) can be a serious problem for some people, but at the same time, it can also be very beneficial to some people. Having SCT, means that you do not have the disease, but are a carrier for the trait. People who have SCT are usually unaffected and live normal lives. On the other hand, people who actually have SCD, can end up dying for having it, and are forced to live irregular, difficult lives.