Anemia

Yes, anemia can cause the production of tear drop-shaped red blood cells. This abnormal shape is associated with conditions like myelofibrosis, where the bone marrow is replaced by fibrous tissue. Anemia in myelofibrosis can lead to the release of immature red blood cells that can have abnormal shapes.

It could be possible, but quite unlikely. The gene is of African origin. Here is how the odds work:

1. If only one parent has the trait, there is a 50% chance that a child of theirs would also just have the trait without having the full-blown disease.

2. If two parents has the trait, then any children would be 25% like to not have the trait at all, 50% likely to be a carrier, and 25% likely to have the full-blown disease.

3. If a person has the disease and the other parent doesn't have the trait at all, then all resulting children would carry the trait but not have the disease.

4. If a person with sickle cell anemia has children with a carrier, then half the children would have the disease, and half would have just the trait.

5. Assuming 2 people with sickle cell anemia are alive long enough to have children together, all their children would have it.

So back to the question. If one parent was White and the other was Black with the sickle cell trait and not the full-blown disease, then they would not have children with the disease, but roughly half would carry it. But if the Black parent was born with the disease (both genes), then none of the children would have it, but all would be carriers. But typically, neither parent would even have the trait, and so none of the children would get it or carry it. Now, lets suppose that two interracial persons produce children together. If by chance they both carried the trait, then the odds are 1 in 4 of having the disease, 1 in 4 of not even carrying it, and a 50% chance of being a carrier.

Sickle cell disease can be a serious and life-threatening condition if not managed properly. Complications such as infections, acute chest syndrome, and stroke can lead to serious health issues and even death. With proper medical care, including regular monitoring and treatment, individuals with sickle cell disease can lead full and productive lives.

yes. thymine replaces adenine in the dna that codes for the amino acid on the 6th position of the beta globin chain resulting in an amino acid change of glutamic acid to valine.

shari

(med student - jamaica)

Down syndrome, Hemophilia, and Sickle cell anemia are all genetic disorders caused by mutations in specific genes. These disorders can lead to various health complications and require ongoing medical management. Additionally, individuals with these conditions may need specialized care and support to maintain their health and well-being.

Sickle cell disease is an example of codominance, not heterozygous dominance. In individuals who are heterozygous for the sickle cell allele, they exhibit a milder form of the disease called sickle cell trait, which demonstrates codominance of the normal and mutant hemoglobin alleles.

Individuals with two recessive alleles have very high rates of reproduction.

One pleiotropic effect of sickle cell syndrome is increased resistance to malaria. The genetic mutation that causes sickle cell disease also confers some protection against malaria infection, as the malaria parasite has difficulty surviving in the altered red blood cells of individuals with sickle cell trait.

they have one normal hemoglobin gene that can produce functional hemoglobin to carry oxygen effectively, compensating for the abnormal hemoglobin produced by the gene for sickle cell disease. This keeps their red blood cells from sickling and causing blockages in blood vessels that lead to symptoms of the disease.

Megaloblastic anemia results from a deficiency of vitamin B12 or folic acid, both of which play a crucial role in DNA synthesis and red blood cell production. This deficiency leads to the production of abnormally large and immature red blood cells, causing anemia.

The dangerous mutation in sickle cell anemia is a point mutation in the HBB gene that results in the substitution of glutamic acid with valine in the beta-globin chain of hemoglobin. This leads to the production of abnormal hemoglobin known as hemoglobin S, which causes red blood cells to take on a sickle shape, leading to various complications such as vaso-occlusive crises, anemia, and organ damage.

In a nutshell, it makes your RBCs (Red Blood cells) sickle shaped. The RBCs can't pick up as much oxygen so you may have trouble breathing. They also collect around the joints causing extreme pain.

Since you did not specify what parental cross you wished to represent this is the best I can do for you. A "normal" male would be represented as XHYo - gametes XH and Yo A male with hemophilia would be represented as XhYo - gametes Xh and Yo A female non-carrier would be represented as XHXH - gametes XH A female carrier would be represented as XHXh - gametes XH and Xh A female with hemophila would be represented as XhXh - gametes Xh

For starters, its immune. Second, sickle cells makes one resistant to malaria if in the heterozygous form (one normal blood cell and one sickle cell allele) but if found in the homozygous form (both alleles for sickle cells) the result is misshapen blood cells that to don't carry enough oxygen through the blood to keep a person alive usually resulting in death.

Sickle-cell anemia is characterised by abnormal haemoglobin which are not the correct shape and cannot carry oxygen.

It is a genetic disease - and a person must have two copies of the gene to have sickle-cell anemia. (Heterozygous individuals, with one copy, are known as having sickle-cell trait - and some of their haemoglobin may be misshapen).

In Africa, malaria is a common disease. It attacks healthy blood cells and uses them to travel throughout the body. However, if one has sickle-shaped blood cells, this makes it harder for the malaria to attach and travel through the body.

A certain substitution in human DNA changes the code for hemoglobin; this ultimately results in sickle-cell anima.

Yes, individuals with sickle cell anemia can live into adulthood with proper care and management of the condition. Regular medical check-ups, adherence to prescribed treatment plans, and healthy lifestyle choices can help improve quality of life and overall life expectancy for those with sickle cell anemia.

Sickle cell disease is an inherited genetic disorder caused by having two copies of the sickle cell gene. When both parents are carriers of the gene, each child has a 25% chance of inheriting the disease. Not every generation will have the disease because it depends on whether the gene is passed down from both parents.

sickle cell trait is inherited from one set of gene alleles from both parents. if you get two traits together it will cause sickle cell anemia which is a disease, sickle cell trait is not a disease.

i dont know what autosomal means!!

i dont know what codominance means!!

The polypeptide chain of hemoglobin designated beta is encoded by the HBB gene. Mutations in this gene can lead to conditions such as sickle cell anemia and beta thalassemia, causing a range of symptoms including anemia, fatigue, and complications related to reduced oxygen transport in the blood. Treatment options for these conditions include blood transfusions, medications, and in some cases, bone marrow transplant.

No, thalassemia is a genetic blood disorder that affects the production of hemoglobin in red blood cells. Blood group and Rh factor are determined by different genetic markers and are not directly linked to thalassemia.

If both U and her husband are carriers of the sickle cell trait, there is a 25% chance that their child will develop sickle cell disease. This is because there is a 50% chance the child will inherit one sickle cell gene from each parent, resulting in the disease.

Yes, sickle-cell anemia is a genetic disorder that affects hemoglobin, causing red blood cells to become rigid and sickle-shaped under certain conditions. This sickling process can lead to blockages in blood vessels, resulting in pain, damage to organs, and other complications.

Sickle cell anemia is caused by a point mutation in the HBB gene, specifically a substitution of adenine for thymine in the sixth codon of the gene, resulting in the production of abnormal hemoglobin known as hemoglobin S.