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Thalassemias are inherited blood disorders that result in abnormal hemoglobin. [7] Symptoms depend on the type of thalassemia and can vary from none to severe. [1] Often there is mild to severe anemia (low red blood cells or hemoglobin) as thalassemia can affect the production of red blood cells and also affect how long the red blood cells live. [1]
Tay–Sachs disease is a genetic disorder that results in the destruction of nerve cells in the brain and spinal cord. [1] The most common form is infantile Tay–Sachs disease, which becomes apparent around the age of three to six months of age, with the baby losing the ability to turn over, sit, or crawl. [1]
Roland Boyd Scott (April 18, 1909 – December 10, 2002) was an American researcher, pediatrician and authority on sickle cell disease. [1] Scott authored a key paper in 1948 describing the incidence of sickle cell in infants that eventually led to the establishment of routine screening for newborns. [1]
Members of BCC are opportunistic human pathogens that most often cause pneumonia in immunocompromised individuals with underlying lung disease (such as cystic fibrosis or chronic granulomatous disease). [2] Patients with sickle-cell haemoglobinopathies are also at risk.
Plasmodium falciparum is a unicellular protozoan parasite of humans, and the deadliest species of Plasmodium that causes malaria in humans. [2] The parasite is transmitted through the bite of a female Anopheles mosquito and causes the disease's most dangerous form, falciparum malaria.
Sickle cell trait causes a change in the haemoglobin molecule in the blood. Normally, red blood cells have a very flexible, biconcave shape that allows them to move through narrow capillaries ; however, when the modified haemoglobin S molecules are exposed to low amounts of oxygen, or crowd together due to dehydration, they can stick together ...
It is possible for a person to have both the gene for hemoglobin S (the form associated with sickle cell anemia) and the gene for hemoglobin C; this state is called hemoglobin SC disease, and is generally more severe than hemoglobin C disease, but milder than sickle cell anemia.
In the earlier stages of the disease, the biopsy typically shows steatosis (deposition of fatty material), increased glycogen in the nucleus, and areas of necrosis (cell death). In more advanced disease, the changes observed are quite similar to those seen in autoimmune hepatitis, such as infiltration by inflammatory cells, piecemeal necrosis ...
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