has anyone ever heard of a caucasion having sickle cell trait?
110246
Sickle cell disease is much more common in certain ethnic groups, but not unheard of in all. Someone who inherits hemoglobin S from one parent and normal hemoglobin (A) from the other parent will have sickle cell trait. (Hemo. S being the one that reduces the oxygen in blood cells)
867443
OK people...here's the lesson for the day...this is an actual bonified case of a genetic trait that is actually inherited through birth....you will notice that it's not some sort of sickness or illness that we all like to pass off as genetic, but it's an actual physiological trait that can be attributed to a genealogical factor...ooooooohhh...amazing isn't it?.......it's just  pigmentation...nothing to worry about...actually kind of unique and cool...a genetic trait stamp like a birthmark, high intelligence or big feet etc...this is what we inherit genetically from our lineage...v cool...
47893
That's sick....\n\nAnyway, I did my assignment on albinism, specifically OCA1-ts albanism.  Do an OMIM search on the NCBI website, that should get you started.  The one mutation I picked was R402Q.
622103
This trait is more common in people of English, Irish or Scotch ancestry than in those of other ethnic groups. The high frequency of hemoglobin D Trait in this population is believed to reflect the large number of Indian wives brought home to England by British troops during Britain's long occupation of India.
783451
The 2 alleles responsible for whether normal or sickle red blood cells are HbA and HbS. The HbS allele (sickle cell gene) is recessive but more exactly, that allele is incompletely recessive (i.e. in the heterozygote HbAHbS, a few sickle red blood cells are still present besides the normal one, shows that HbS gene are still expressed at small rate). The HbS induces the polymerization of hemoglobin in red blood cells, leading to abnormal sickle shape of the cells, making it very difficult for these red blood cells to pass through the blood vessels and stuck there.\n\nOne person is called suffering from sickle cell anemia if they have the HbSHbS form, i.e. the homozygous recessive. In the HbAHbS the few sickle red blood cells are not enough to cause symptoms. \n\nOne interesting thing about this disease is that, while the HbSHbS form would be dangerous because the red blood cells cannot carry oxygen to cells and stuck in the blood vessels, the carriers (HbAHbS) would have advantage in malaria region. Since the malaria parasite spends parts of its life in red blood cells, these parasite cause the abnormal sickle cells to rupture, moreover, the polymerization of Hb disables the parasites to digest Hb. The white blood cells also kill the parasite better when they come to kill the stuck sickle cells. That why people with HbAHbS form have a higher fitness to the malaria environment than people with normal red blood cells.
30998
dyeing them if not that way than through family genes
600548
Because it's a genetically recessive disease; both parents need to have it in order to have a child with the disease. Also, sickle cell anemia hurts your body's capacity to carry oxygen, so people afflicted tend to have less children, so it tends not to spread amongst the population.\n\nBoth these make it quite rare in the West. But in some parts of Africa, where malaria strikes and kills millions of people, sickle cell anemia is actually a good disease to have, because it protects you against malaria. So people with it actually have *more* children than people without, so the damaged gene spreads and survives!
247635
How Do People Get Thalassemia?\n\n Thalassemia is an inherited condition. The genes received from one's parents before birth determine whether a person will have thalassemia. Thalassemia cannot be caught or passed on to another person. The clinical severity of thalassemia varies tremendously depending on the exact nature of the genes that a person inherits.\n\nHow Are Genes Inherited?\n At the time of conception, a person receives one set of genes from the mother (egg) and a corresponding set of genes from the father (sperm). The combined effects of many genes determine some traits (hair color, and height for instance). Traits determined by a combination of genes often have gradations in magnitude (the difference between Michael Keaton and Kareem Abdul-Jabbar, for instance). Other characteristics are determined by a single gene pair (a person's sex, for instance). A person is either a biological male or female.\n\n The inheritance pattern is complicated in patients with thalassemia because two sets of genes on different chromosomes cooperate to produce hemoglobin. A defect anywhere in this complex can produce thalassemia. The expression of thalassemia, therefore, more closely resembles that of height, with gradations in effect.\n\nInheritance of Hemoglobin\n The genes involved in thalassemia control the production of a protein in red cells called hemoglobin. Hemoglobin binds oxygen in the lungs and releases it when the red cells reach peripheral tissues, such as the liver. The binding and release of oxygen by hemoglobin is essential for survival.\n\nEach hemoglobin molecule contains four subunit proteins. Two of the subunit proteins are called alpha and two are called beta. Hemoglobin properly binds and releases oxygen only when two alpha subunits are connected to two beta subunits. A pair of genes located on chromosome #16 controls the production of the alpha subunits of hemoglobin. A single gene located on chromosome #11 controls the production of the hemoglobin beta subunit (Figure 1).\n\n All cells contain pairs of idential chromosomes, one from the father and one from the mother. Each chromosome contains thousands of genes lined up in sequence. As shown in Figure 1, each person has two beta globin genes, one from the father and one from the mother. Since each chromosome #16 has two alpha globin genes, each person has a four of these genes. One chromosome #16 comes from the father, who therefore contributes two alpha globin genes to the offspring. One chromosome #16 comes from the mother who also contributes two alpha globin genes to the offspring.\n\n A complete hemoglobin molecule has four subunits: two alpha and two beta. The two beta globin genes contribute equally to the production of beta globin subunit protein. The alpha globin genes together produce an amount of alpha globin protein that exactly equals the beta globin protein. Since there are four alpha globin genes compared to two beta globin genes, each alpha globin gene produces only about half as much protein as a beta globin gene. These keeps the overall production of subunits equal from each set of chromosomes (Figure 1).\n\n Thalassemia occurs when one or more of the genes fails to produce protein, leading to a shortage of one of the subunits. If one of the beta globin genes fails, the condition is called beta thalassemia. Beta thalassemia, therefore, is due to a shortage of beta subunits. If an alpha globin gene fails, the condition is called alpha thalassemia. In this case, a shortage of alpha subunits occurs..............
1079358
Sickle cell trait carriers.\nNot sickle cell anemia.\nThe carriers of this trait are resistant from Plasmodium falciprium (aka malaria).\nThis trait is prevalent amongst the African race and provides resistance and gives us another example of evolution.\nAnother example of a helpful mutation happens in Europeans and European Americans, this is the delta-32 mutation.  Having this mutation provides resistance to the bubonic plague and HIV.  This occurs in your immune cells called macrophages that close the membrane that doesn't allow this bacteria and virus to enter the macrophage.  If you have this mutation, you'll never get HIV/AIDS or Bubonic Plague.\n\nLike it or not:\nEvolution has happened, will happen and will continue to happen.
623305
Sickle-cell anemia is encountered almost exclusively in people of African descent, although there are always exceptions.  The reason sickle-cell anemia is so common (compared to other genetic disorders) in certain populations is that carriers of the gene (i.e. people who have only one copy of it) have slightly oddly shaped red blood cells, which don't cause any problems for them but aren't so great for the parasite that causes malaria.  Since carriers are resistant to malaria, the gene that causes sickle-cell is extremely common only within populations from regions where malaria is endemic.  Since malaria is quite prevalent in many regions of Africa, sickle-cell is also prevalent in people whose ancestry traces back to those regions.  Sickle-cell can pop up anywhere, in any population through random mutation (if I remember correctly, it's a single nucleotide mutation), but without malaria to give heterozygous individuals (i.e. carriers) an advantage, it does not become nearly as common as it did in African populations.
386781
Human parthenogenesis has never been recorded for certain.  But, then again, chances are, if it has happened, nobody would notice.  Only recently has genetic testing been available to test it, I keep expecting an example to turn up eventually.
585548
sickle cell is more biology based. Chemistry would be medication and production of pharmaceutical goods.\nEquations would be easier to find for that.\nGood luck.
29588
A sex-linked trait is typically carried on the X chromosome, although it can also be carried on the Y-chromosome instead.  Common examples include color-blindness and hemophillia.
360951
It's very possible. My best friend is Native American, and she is as blue eyed/blonde as them come. Recessive genes can toss you through a loop. Give him the benefit.
989486
Sickle cell disease is a general term for a group of genetic disorders caused by sickle hemoglobin (Hgb S or Hb S). In many forms of the disease, the red blood cells change shape upon deoxygenation because of polymerization of the abnormal sickle hemoglobin. This process damages the red blood cell membrane, and can cause the cells to become stuck in blood vessels. This deprives the downstream tissues of oxygen and causes ischemia and infarction. The disease is chronic and lifelong. Individuals are most often well, but their lives are punctuated by periodic painful attacks. In addition to periodic pain, there may be damage of internal organs, such as stroke. Lifespan is often shortened. It is common in people from parts of the world where malaria is or was common, especially in West Africa or in descendents of those peoples. Sickle cell disease can occur in any individual of any color or ethnicity, however.\n\n"Sickle cell anemia" is the name of a specific form of sickle cell disease in which there is homozygosity for the mutation that causes Hgb S. Other forms of sickle cell disease include sickle-hemoglobin C disease, sickle beta-plus-thalassemia, and sickle beta-zero-thalassemia. Unlike sickle cell anemia, these other forms of sickle cell disease are compound heterozygous states in which the person has only one copy of the mutation that causes Hgb S and one copy of another abnormal hemoglobin gene. It is important to know that "sickle cell anemia" is the proper name of a specific type of "sickle cell disease", and that "sickle cell disease" is a non-specific term. Because the different forms of sickle cell disease are quite different, one must be sure to specify the exact form of the disease in question. The disease was originally called sickle-cell anemia but this name has fallen out of favor in medical contexts because anemia is not the only symptom of the disease.\n\nSigns and symptoms\n\nPatients with sickle cell anemia have steady-state or baseline anemia that varies in severity, with hemoglobin levels of 6-9 g/dl typical. Reticulocyte counts are elevated, reflecting new red blood cells replacing the rapidly destroyed older cells - red blood cell life span is markedly reduced in this disease. Often, the white blood cell and platelet counts are elevated, and these cells may contribute to vaso-occlusion.\n\nVaso-occlusive crisis\n\nVaso-occlusive crisis is caused by sickle shaped red blood cells that obstruct capillaries and restrict bloodflow to an organ, resulting in ischemia, pain, and organ damage.\n\nBecause of its narrow vessels and function in clearing defective red blood cells, the spleen is frequently affected. It is usually infarcted before the end of childhood in individuals suffering from sickle cell anemia. This autosplenectomy increases the risk of infection from encapsulated organisms; preventive antibiotics and vaccinations are recommended for those with such asplenia. Liver failure may also occur with time.\n\nBone is also a common target of vasoocclusive damage, especially when the bone is particularly weight-bearing. Such damage may result in avascular necrosis (especially of the femur) and bone deterioration. The pain experienced by sickle-cell patients is also due to the bone ischemia.\n\nA recognized type of sickle crisis is the acute chest crisis, a condition characterized by fever, chest pain, hard breathing, and pulmonary infiltrate on chest x-ray. Given that pneumonia and intra-pulmonary sickling can both produce these symptoms, the patient is treated for both conditions. Treatment consists of admission, oxygen, close monitoring, and intravenous antibiotics.\n\nOther sickle-cell crisis\n\nAplastic crisis. An acute worsening of the patient's baseline anemia producing pallor, tachycardia, and fatigue. This crisis is triggered by parvovirus B19, which directly affects erythropoiesis (production of red blood cells). Reticulocyte counts drop dramatically dur
539915
Hbf, is the type oh Hemoglobin that's supposed to be found \n(In high percentages) in fetuses, hence the "F", and almost 0% in adults. Sickle cell anemia is inherited as an autosomal (meaning that the gene is not linked to a sex chromosome) recessive condition whereas sickle cell trait is inherited as an autosomal dominant trait. This means that the gene can be passed on from a parent carrying it to male and female children. In order for sickle cell anemia to occur, a sickle cell gene must be inherited from both the mother and the father, so that the child has two sickle cell genes. \n\nThe inheritance of just one sickle gene is called sickle cell trait or the "carrier" state. Sickle cell trait does not cause sickle cell anemia. Persons with sickle cell trait usually do not have many symptoms of disease and have normal hospitalization rates and life expectancies.It's supposed to carry both recessive genes to have the disease.\nSickling of the red blood cells in patients with sickle cell anemia results in cells of abnormal shape and flexibility. The sickling is promoted by conditions which are associated with low oxygen levels, increased acidity, or low volume (dehydration) of the blood. These conditions can occur as a result of injury to the body's tissues, dehydrating states, or anesthesia. \n\n This disease occurs exclusively in Black people for an unknown reason.
9126
Sickle cell anemia pre-dominately occurs in African-Americans; yet, also occurs in people of Mediterranean and Middle Eastern descent.  I was reading on a website that said 1 in 12 African -Americans carry the recessive gene that causes the sickle cell disorder.  Thankfully, stem cell researchers have and are currently developing more treatments & cures for the disorder.