Silicon Investor (SI) -- The First Internet Community

STOCKTALK

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor. We ask that you disable ad blocking while on Silicon Investor in the best interests of our community. If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.

Politics : Sharks in the Septic Tank -- Ignore unavailable to you. Want to Upgrade?

To: epicure who wrote (71888)	8/6/2003 4:31:37 PM
From: Neocon	Read Replies (2) \| Respond to of 82486

I would be very curious to know how this is adaptive: Sickle cell anemia is an inherited disease in which the red blood cells, normally disc-shaped, become crescent shaped. As a result, they function abnormally and cause small blood clots. These clots give rise to recurrent painful episodes called "sickle cell pain crises". Causes, incidence, and risk factors Return to top Sickle cell anemia is caused by an abnormal type of hemoglobin (oxygen carrying molecule) called hemoglobin S. It is inherited as an autosomal recessive trait -- that is, it occurs in someone who has inherited hemoglobin S from both parents. Someone who inherits hemoglobin S from one parent and normal hemoglobin (A) from the other parent will have sickle cell trait. Approximately 8% of African Americans have sickle cell trait. Someone who inherits hemoglobin S from one parent and another type of abnormal hemoglobin from the other parent will have another form of sickle cell disease, such as sickle cell-b 0 thalassemia, hemoglobin SC disease, or sickle cell-b + thalassemia. Someone with sickle cell trait or these forms of sickle cell disease will usually have no symptoms or only mild ones. However, some of these conditions can cause symptoms similar to sickle cell anemia. Sickle cell disease is much more common in certain ethnic groups, affecting approximately one out of every 500 African Americans. Because people with sickle trait were more likely to survive malaria outbreaks in Africa than those with normal hemoglobin, it is believed that this genetically aberrant hemoglobin evolved as a protection against malaria. Although sickle cell disease is inherited and present at birth, symptoms usually don't occur until after 4 months of age. Sickle cell anemia may become life-threatening when damaged red blood cells break down (hemolytic crisis), when the spleen enlarges and traps the blood cells (splenic sequestration crisis), or when a certain type of infection causes the bone marrow to stop producing red blood cells (aplastic crisis). Repeated crises can cause damage to the kidneys, lungs, bones, eyes, and central nervous system. Blocked blood vessels and damaged organs can cause acute painful episodes. These painful crises, which occur in almost all patients at some point in their lives, can last hours to days, affecting the bones of the back, the long bones, and the chest. Some patients have one episode every few years, while others have many episodes per year. The crises can be severe enough to require admission to the hospital for pain control and intravenous fluids. Many manifestations of this disease are a result of the fragility and inflexibility of the sickle red blood cells. When patients experience dehydration, infection, and low oxygen supply, these fragile red blood cells assume a crescent shape, causing red blood cell destruction and poor flow of these blood cells through blood vessels, resulting in a lack of oxygen to the body's tissues. Symptoms Return to top joint pain and other bone pain fatigue breathlessness rapid heart rate delayed growth and puberty susceptibility to infections ulcers on the lower legs (in adolescents and adults) jaundice bone pain attacks of abdominal pain fever Additional symptoms that may be associated with this disease: bloody urine (hematuria) excessive urination, excessive volume thirst, excessive unwanted painful erection (priapism; this occurs in 10-40% of men with the disease) chest pain poor eyesight/blindness Signs and tests Return to top Common signs include: paleness yellow eyes/skin growth retardation nlm.nih.gov

To: epicure who wrote (71888)	8/6/2003 4:33:41 PM
From: Neocon	Read Replies (1) \| Respond to of 82486

Maybe you can explain how Tay- Sachs is adaptive,too?: Tay-Sachs Disease What Is Tay-Sachs Disease? Tay-Sachs disease is a fatal inherited disease of the central nervous system. The most common form of the disease affects babies. Affected babies appear healthy at birth and seem to develop normally for the first few months of life. After this time, development slows and symptoms begin. Sadly, there is no effective treatment for these babies. Babies with Tay-Sachs lack an enzyme (protein) called hexosaminidase A (hex A) necessary for breaking down certain fatty substances in brain and nerve cells. These substances build up and gradually destroy brain and nerve cells, until the entire central nervous system stops working. Symptoms of classical Tay-Sachs disease first appear at 4 to 6 months of age when an apparently healthy baby gradually stops smiling, crawling or turning over, loses its ability to grasp or reach out and, eventually, becomes blind, paralyzed and unaware of its surroundings. Death occurs by age 5. Who Is at Risk of Tay-Sachs Disease? Tay-Sachs disease occurs most frequently in descendants of Central and Eastern European (Ashkenazi) Jews. About one out of every 30 American Jews carries the Tay-Sachs gene. Some non-Jewish individuals of French-Canadian ancestry (from the East St. Lawrence River Valley of Quebec), and members of the Cajun population in Louisiana, are at similarly increased risk. These groups have about 100 times the rate of occurrence of other ethnic groups. The juvenile form of Tay-Sachs, however, may not be increased in these groups. How Is the Disease Transmitted? Only through heredity. A Tay-Sachs carrier has one normal gene for hex A and one Tay-Sachs gene. The carrier does not have the illness and leads a normal, healthy and full life. However, when two carriers become parents: There is a one-in-four chance that any child they have will inherit a Tay-Sachs gene from each parent and have the disease. There is a one-in-four chance that the child will inherit the normal gene from each parent and be completely free of the disease and the Tay-Sachs gene. There is a two-in-four chance that the child will inherit one of each kind of gene and be a carrier like the parents and free of disease. If only one parent is a carrier, none of their children can have the disease, but each child has a 50-50 chance of inheriting the Tay-Sachs gene and being a carrier. Are There Other Forms of Tay-Sachs Disease Besides the Classical Type That Affects Babies? The classic infantile type of Tay-Sachs is the most common. However, there are other rare deficiencies of the hex A enzyme that sometimes are included under the name of Tay-Sachs disease. These often are referred to as juvenile, chronic and adult-onset forms of hex A deficiency. Affected individuals have low levels of the hex A enzyme that is missing entirely in the classical, infantile form. This may help explain why symptoms begin later in life and, generally, are milder than in the classical, infantile Tay-Sachs disease. Children with juvenile hex A deficiency develop symptoms between the ages of 2 and 5 that resemble those of the classical, infantile form. Although the course of the disease is slower, death generally occurs by age 15. Symptoms of chronic hex A deficiency also may begin by age 5, but are far milder than those that characterize the infantile and juvenile forms. Mental abilities, vision and hearing remain intact; but there may be slurred speech, muscle weakness, muscle cramps, tremors, unsteady gait and, sometimes, mental illness. Individuals with adult-onset hex A deficiency experience many of the same symptoms as individuals with the chronic form, but the symptoms begin later in life. Is There Any Treatment for Tay-Sachs? Tragically, there is no cure, and no treatment that will prevent the disease from running its course. Affected children can only be made as comfortable as possible. marchofdimes.com