Although the wide majority of Alpha 1's are of Northern European decent, most of us are not of one pure race. If he is an Alpha then both of his parents would have to be carriers of the gene. A simple blood test can determine if he was an Alpha and I don't know if that was done. Alpha 1 deficiency can cause either chronic COPD or liver disease.
No one knows if Michael Jackson had Alpha-1 Antitrypsin Deficiency.
The only source for the claim is Ian Halperin, a writer who did a biography of Jackson. Halperin provided no evidence whatever for this claim, and Jackson's spokesman denied it as "a total fabrication."
Alpha-1 is considered rare in African Americans. However, the Alpha-1 Foundation recently awarded a grant to study the high rate of lung disease in African Americans, and to test them for Alpha-1 Antitrypsin Deficiency.
Emphysema is primarily caused by long-term exposure to irritants that damage the lungs, with smoking being the most common risk factor. However, non-smokers can develop emphysema due to factors such as exposure to air pollution, occupational dust and chemicals, and genetic conditions like alpha-1 antitrypsin deficiency. Additionally, chronic respiratory infections can contribute to lung damage over time. It's essential to maintain lung health by avoiding known irritants and seeking medical care for persistent respiratory issues.
She is an honorary member of Alpha Kappa Alpha. and that is because her grandmother is a member of Alpha Kappa Alpha {how do i know , i grew up with her}
An alpha particle is identical to the nucleus of Helium atom
I'm pretty sure its alpha.
The equation for the alpha decay of 222Rn is: 86222Rn --> 84218Po + 24He Where He represents the alpha particle, which can also be viewed as a Helium nucleus.
no
The number of Americans with this deficiency is relatively small, probably no greater than 70,000
People with this type of emphysema have a hereditary deficiency of a blood component, an enzyme inhibitor called alpha-1-antitrypsin
Alpha-1 antitrypsin (AAT) is a condition whereby the body suffers a deficiency of the protein required to protect the liver and the lungs from damage, which may lead to liver diseases or emphysema.
Alpha-1 Antitrypsin Deficiency is a genetic disorder that is passed along through generations. This is a deficiency in a protein of the lungs and the liver. If left untreated, it can ultimately lead to lung and liver disease.
The Alpha 1 Antitrypsin Deficiency means that the body does not make enough protein to protect the liver and lungs from damage. AAT is given to patients to help them produce some protein. If the patient smokes they are advised to quit.
It is thought that every 1:2000 Caucasian births results in someone who is genetically 'alpha-1 antitrypsin deficient'. This puts the potential deficient population in the US at about 100,000 even though only a fraction of that number has been identified. For more information go to the related link below.
Alpha-1 antitrypsin was discovered by Dr. Laurell and Dr. Eriksson in 1963. They identified it as a serum protein and named it alpha-1-antitrypsin based on its ability to inhibit the enzyme trypsin.
Alpha 1-antitrypsin deficiency primarily affects the lungs and liver, leading to conditions such as emphysema and liver disease. While it is not directly linked to memory loss, the associated complications, such as chronic hypoxia from lung issues or hepatic encephalopathy from liver dysfunction, could potentially contribute to cognitive impairments. Therefore, while memory loss is not a direct symptom of the deficiency itself, secondary effects from related health issues may impact cognitive function.
It is a blood component that breaks down infection-fighting enzymes such as elastase
Alph-1-antitrypsin, produced in the liver, is a protease inhibitor. It inhibits Factor XIa, thrombin, kallikrein, plasmin, and tPA in the coagulation pathway. It is the major inhibitor of FXIa.
Excess secretion of trypsin can lead to the degradation of elastic fibers in lung tissue, contributing to the development of emphysema. Normally, trypsin is regulated by alpha-1 antitrypsin, which protects lung tissue from excessive proteolytic activity. When there is an imbalance, either due to genetic factors like alpha-1 antitrypsin deficiency or increased trypsin activity, it can result in the destruction of alveolar walls, leading to emphysema. This condition impairs lung function and reduces respiratory efficiency.