Several major Universities whose main function is Technology, along with the Medical Schools associated with teaching in the Children's Hospitals have begun joining forces using Nanotechnology to alter the genetics of the sickle cell trait. Among them is a collaborative effort between GA Institute of Technology, Emory University Medical School, and Children's Health Care Systems of Atlanta. Once this is accomplished, plans are already in the works to move on to another deadly disease initiated with inherited genes: Cystic Fibrosis. This is an excellent collaborative use of each genre's best abilities: cooperation vs competition.
I earlier times this may have been negatively associated with eugenics, however that connotation is now being transformed with the positive aspects of actually changing genetics at the microcellular level to rid populations of certain killer traits, rather than attempts at 'perfecting the human race,' as in the despicable times of Hitler. This is not a genocidal experiment, but one aimed at saving lives of painful and deathly diseases, remembering sickle cell trait is mostly among Blacks.
To get a clearer picture of why the allele is still present, just remember what the Hardy-Weinberg principle predicts:
both allele and genotype frequencies in a population remain constant; that is, they are in equilibrium from generation to generation unless specific disturbing influences are introduced. Those disturbing influences include non random mating, mutations, selection, limited population size, "overlapping generations," random genetic drift, gene flow and meiotic drive.
Since the homozygous recessive (when the Anaemia is actually expressed) and heterozygous condition do not affect mating probabilities, the allele will naturally remain within the population.
A gene mutation can cause sickle cell anemia, a type of hemolytic anemia where red blood cells become crescent-shaped and rigid, leading to reduced oxygen delivery, pain, and organ damage.
A slide of sickle cell anemia would typically show red blood cells that are shaped like a sickle or crescent due to the presence of abnormal hemoglobin. These misshapen cells can lead to blockages in blood vessels, causing tissue damage and pain. Additionally, the sickle cells are more fragile and have a shorter lifespan than normal red blood cells.
The gene associated with sickle cell anemia is HBB, which is located in region 15.5 on the short arm of chromosome 11. There are many variations that can cause sickle cell, but primarily it is caused by the hemoglobin variant Hb S. According to the human genome project website: "the hydrophobic amino acid valine takes the place of hydrophilic glutamic acid at the sixth amino acid position of the HBB polypeptide chain. This substitution creates a hydrophobic spot on the outside of the protein structure that sticks to the hydrophobic region of an adjacent hemoglobin molecule's beta chain. This clumping together (polymerization) of Hb S molecules into rigid fibers causes the "sickling" of red blood cells." In a nutshell, when the hydrophobic (water fearing) amino replaces a hydrophilic one (water loving) on the protein chain, it creates a spot that sticks to another similar mutated gene, and they clump together, creating a sickle shaped cell. Looking at the location and incidence rates of sickle cell amenia, scientists believe that because malaria rates are high in the region, the body has created this defense against the disease -- an evolutionary self defense. Hope that helps :-)
Pleiotropy describes the genetic effect of a single gene on multiple phenotypic traits. The underlying mechanism is that the gene codes for a product that is for example used by various cells, or has a signalling function on various targets. A classic example of pleiotropy is the human disease PKU (phenylketonuria). This disease can cause mental retardation and reduced hair and skin pigmentation, and can be caused by any of a large number of mutations in a single gene that codes for an enzyme (phenylalanine hydroxylase) that converts the amino acid phenylalanine to tyrosine, another amino acid. Depending on the mutation involved, this results in reduced or zero conversion of phenylalanine to tyrosine, and phenylalanine concentrations increase to toxic levels, causing damage at several locations in the body. PKU is totally benign if a diet free from phenylalanine is maintained.
Human activities affect water cycle. It should be maintained by afforestation, reducing pollution.
the only human adaptation to malaria is sickle-cell anemia true?
Parkinsons Disease or Sickle Cell Anemia.
Huntington's Poly Cystic Ovary Sickle Cell Anemia Etc, Etc, etc
Heterozygous induviduals pass the dominant and recessive alleles to offspring
A gene mutation can cause sickle cell anemia, a type of hemolytic anemia where red blood cells become crescent-shaped and rigid, leading to reduced oxygen delivery, pain, and organ damage.
NONE.
A slide of sickle cell anemia would typically show red blood cells that are shaped like a sickle or crescent due to the presence of abnormal hemoglobin. These misshapen cells can lead to blockages in blood vessels, causing tissue damage and pain. Additionally, the sickle cells are more fragile and have a shorter lifespan than normal red blood cells.
None. =]
Assuming you mean human red blood cells (RBC), there are several "special" things about RBCs. RBCs do not have a nucleus, and they have a distinct shape-biconcave disks. That means they are shaped sort of like a donut, but without an actual hole in the center, just indentations. Sickle-cell anemia, for example, is so named because the RBCs of people with sickle-cell anemia are shaped like sickles. These unusually shaped cells have a harder time moving through the capillaries and transporting oxygen.
Sickle-cell disease
Some examples of deleterious traits in humans include genetic disorders such as cystic fibrosis, sickle cell anemia, and Huntington's disease. These traits can decrease an individual's lifespan or quality of life.
It sucks the blood of the host human from its intestine and may cause severe anemia.