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Sickle Cell Disease:     more books (100)

Troubled Dream of Genetic Medicine Ethnicity & Innovation in Tay-Sachs, Cystic Fibrosis, & Sickle Cell Disease by KeithWailo&StephenPemberton, 2006 The Sickle Cell Disease Patient by Felix I.D. Konotey-Ahulu, 1996-12-31 Advances in the Pathophysiology, Diagnosis, and Treatment of Sickle Cell Disease: Proceedings of the Tenth Annual Postgraduate Conference on Sickle Cell Disease Sickle Cell Disease: A Guide for Families by Elizabeth Anionwu, H. Jibril, 1992-01 Sickle Cell Disease: Screening, Diagnosis, Management, and Counseling in Newborn and Infants (Clinical Practice Guideline) by Jeanne A. Smith, Thomas R. Kinney, 1997-01 Sickle Cell Disease (Hematology/Oncology Clinics of North America, 10:6) by ed. Samuel Charache and Cage S. Johnson, 1996 ADOLESCENTS WITH SICKLE CELL DISEASE: Determinants of Support Group Attendance and Satisfaction.: An article from: Health and Social Work by Joseph Telfair, Marilyn M. Gardner, 2000-02-01 Development of Therapeutic Agents for Sickle Cell Disease: INSERM Symposium Proceedings (Inserm symposium ; 9) Sickle Cell Disease. A Guide for Patients, Carers and Health Workers by Ian Franklin, 1990 The handbook on the psychology of hemoglobin-S: A perspicacious view of sickle cell disease by Samuel Rayford McElroy, 1980 Sickle Cell Disease: Diagnosis, Management, Education and Research The clinical features of sickle cell disease (Clinical studies) by Graham R Serjeant, 1974 Sickle Cell Disease (Oxford Medical Publications) by Graham R. Serjeant, Beryl E. Serjeant, 2001-06-24 Comparative Clinical Aspects of Sickle Cell Disease (The University of Chicago Sickle Cell Center Hemoglobin Symposia)

lists with details

21. Pediatric Hematology/Oncology Clinic At The U-M Cancer Center
    Affiliated with Mott Children's Hospital, the UMCC Pediatric Cancer Clinic at the University of Michigan treats pediatric cancers, as well as sickle cell disease, chronic neutropenias and chronic granulomatous disease.  
    http://www.cancer.med.umich.edu/clinic/pedclinic.htm
    
    Extractions: The Division of Pediatric Hematology/Oncology Pediatric Hematology / Oncology Clinic The Pediatric Hematology / Oncology Clinic treats patients with pediatric solid tumors, including neuroblastomas rhabdomyosarcomas Wilm's tumors and brain tumors , as well as patients with l ymphomas leukemias and other childhood cancers . Patients with coagulation disorders and sickle cell anemia are also seen in the clinic, since it is part of The Division of Pediatric Hematology/Oncology The U-M has the largest pediatric oncology research effort in Michigan. Studies are ongoing to better understand genetic mechanisms underlying neuroblastoma, acute leukemia and brain tumors. Other studies are directed toward improving patients' own defenses against cancer. The U-M program is one of only a few in the United States to hold a training grant in Pediatric Hematology, which allows the program to train future academicians in clinical care and research involving childhood hematologic and oncologic diseases. About the Clinic Appointments Physicians and Staff Pediatric Cancer Treatment Information ... Support See Also:

22. Sickle Cell Society
    Latest Events The Latest Events organised by SCS. A New NCEPOD Study sickle cell disease and Thalassaemia. What is Sickle Cell Anaemia?  
    http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

23. MedlinePlus: Sickle Cell Anemia
    (sickle cell disease Association of America); What Is sickle cell disease? Law and Policy; sickle cell disease Americans with Disabilities Act (Georgia  
    http://www.nlm.nih.gov/medlineplus/sicklecellanemia.html
    
    Extractions: From the National Institutes of Health Sickle Cell Anemia (National Heart, Lung, and Blood Institute) Overviews Frequently Asked Questions (Sickle Cell Disease Association of America) Sickle Cell Disease (March of Dimes Birth Defects Foundation) What Is Sickle Cell Disease? (Sickle Cell Disease Association of America) What Is Sickle Cell Disease? (Dolan DNA Learning Center) Diagnosis/Symptoms Blood Smear (American Association for Clinical Chemistry) Complete Blood Count (American Association for Clinical Chemistry) Hemoglobin Variants (American Association for Clinical Chemistry) Treatment Blood and Marrow Stem Cell Transplantation Also available in: Spanish Bone Marrow and Cord Blood Stem Cell Transplant (Georgia Comprehensive Sickle Cell Center at Grady Health System) Prevention/Screening Genetic Counseling (Nemours Foundation) Genetic Testing for Newborns at Increased Risk (American Association for Clinical Chemistry) Newborn Screening Tests (March of Dimes Birth Defects Foundation)

24. James R. Clark Sickle Cell Foundation Web Page
    Foundation working to optimize the social, psychological and physiological well being of residents with sickle cell disease through the provision of services to individuals, families, and communities.  
    http://www.midnet.sc.edu/jrcsc
    
    Extractions: Email: jrcsc@bellsouth.net The James R. Clark Memorial Sickle Cell Foundation, Inc. was chartered in 1972 in Columbia, South Carolina as a comprehensive community-based health organization to serve the needs of patients with sickle cell disease. The foundation is named after James R. Clark, MD, who was a founder and advocate for patients with the sickle cell disease. The mission of the James R. Clark Memorial Sickle Cell Foundation is to optimize the social, psychological and physiological well being of residents with sickle cell disease with in the fifteen county area of the State that we serve. This mission shall be accomplished through the provision of comprehensive services to individuals, families, and communities and shall be further enhanced by collaboration with appropriate federal, state, and local resources and through the involvement of volunteers and contributors. A staff of thirty-one (31) full-time, part-time and paid staff members assure accessible services for our clients.

25. Welcome To The American Sickle Cell Anemia Association
    accumulated over time from various factual sources, medical journals and general entities about sickle cell anemia and its disease variants.  
    http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

26. Passive Tobacco Smoke Increases Complications In Children With Sickle Cell Disea
    Research finds hat children with sickle cell disease who are exposed to tobacco smoke in the home have more complications from the disease than those who live in a smokefree environment.  
    http://www.eurekalert.org/pub_releases/2003-12/uocd-pts121603.php
    
    Extractions: University of California, Davis - Medical Center (SACRAMENTO, Calif.) Physicians and researchers at the UC Davis School of Medicine and Medical Center found that children with sickle cell disease who are exposed to tobacco smoke in the home have more complications from the disease than those who live in a smoke-free environment. The study was published in the December issue of the Archives of Pediatrics and Adolescent Medicine. "Exposure to environmental or passive tobacco smoke increased the risk of sickle cell crisis by 90 percent, and was not influenced by other factors known to increase complications, such as age of the patient or type of sickle cell disease," said Daniel C. West, associate professor of pediatrics at UC Davis and lead author of the study. "Exposure to tobacco smoke has a tremendous impact on children with sickle cell disease. In fact, the study suggests that removing passive tobacco smoke from the home might not only reduce the suffering of children with sickle cell disease, but also reduce the cost of medical care." Sickle cell disease is a hereditary disease that affects hemoglobin, the protein in red blood cells that carries and delivers oxygen to tissues. The presence of sickle hemoglobin can lead to damaged and misshapen red blood cells that do not flow normally through blood vessels and deliver less than the normal amount of oxygen to peripheral tissues. These abnormalities can cause episodes of severe pain, known as sickle cell crises, and life-threatening damage to vital organs, such as the lungs and the brain.

27. USATODAY.com - Disease Experts Study May Bring Sickle Cell
    sickle cell disease got its name because a defect in hemoglobin, which carries oxygen, turns blood cells into hard sickles rather than soft  
    http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

28. USA Medical Center
    Teaching hospital for the University of South Alabama offering care for trauma, burns, cancer, cardiovascular disease, strokes, organ transplant and sickle cell disease.  
    http://www.southalabama.edu/usamc/
    
    Extractions: FAX: (251) 470-1672 Home Centers for Patient Care Directions Billing ... Contact Us The University of South Alabama Medical Center is a regional referral center for south Alabama, southern Mississippi and the panhandle of Florida. As the primary teaching facility for the University of South Alabama College of Medicine, the 406-bed acute care hospital offers many unique programs and services for adult patients. Our centers of excellence provide services and resources that enhance the health of the community and support the hospital's mission of health care, education and research. For more information about healthcare services available at USA Medical Center, contact Bob Lowry , Office of Public Relations. Visiting Hours Hospital Stay Preparation Patient Handbook Volunteer Opportunities ... University of South Alabama - Mobile Alabama 36688-0002 / 1 (251) 460-6101

29. Sickle Cell Information Center Home Page
    How May We Serve You? What is sickle cell disease? Health Care Providers Online Resources and Guidelines  
    http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

30. Sickle Cell Anemia
    Treatment of sickle cell disease The primary goal of therapy is to reduce the frequency, duration, and severity of the sickle cell crisis episodes and to  
    http://radlinux1.usuf1.usuhs.mil/rad/home/cases/sickle.html
    
    Extractions: Ironically, the sickle cell trait (the heterozygous HgbSA - not the homozygous HgbSS) seems to have a protective effect against the malaria parasite. By the time many patients reach adulthood, there is often objective evidence of anatomic and/or functional damage to various tissues due to the cumulative effects of recurrent vasoocclusive (clotting) episodes. However, the course of the disease is variable from patient to patient. Learn More About Sickle Cell Anemia - 1 The first is most commonly seen only in sickle cell anemia. Marrow hyperplasia crowds and thins the bone trabeculae which results in bone weakness and osteoporosis. Bone softening at the centra of the vertebral bodies of the spine occurs in 70% of patients; a biconcave shape results as the intervertebral disks push into the softened bone. Infarction on the vertebral bodies may also result in partial or complete collapse of the central portion as well. The biconcave, or "fish mouth" vertebrae (due to compression of the vertebral endplates above and below the disk space) are virtually pathognomonic of sickle cell disease. Such changes are evident on the enclosed chest X-rays.

31. CNN.com - Health - Devastation Of Sickle Cell Disease Chronicled - February 22,
    http://cnn.com/2001/HEALTH/conditions/02/22/sickle.cell.anemia/index.html
    
    Extractions: CNN.com Health Writer ATLANTA, Georgia (CNN) - Although research continues, sickle cell anemia remains an "orphan disease" attracting little notice despite its harvest of pain and early death. But a new film documentary may help to educate viewers about the disease, which affects about 80,000 people in the United States and millions worldwide. Called "Sickle Cell: The Forgotten Disease," the film will air at 10 p.m. EST on the Discovery Health Channel. It is being co-produced by the Dr. Spock Company. "It's hard to get funding or people interested in trials," said Dr. James Eckman, director of the Georgia Comprehensive Sickle Cell Center at Grady Health System. "But because this is a lifelong, chronic problem, it has a greater impact." CONDITION CLINIC Sickle Cell disease A genetic disorder, sickle cell disease attacks red blood cells, making them rigid and distorting their normally round shape into crescents and points. These misshapen cells can easily clog tiny blood vessels and deprive organs and tissues of vital oxygen, causing intractable pain crises. In addition, children with sickle cell are more prone to stroke, pneumonia, infection and other long-term complications.

32. CNN - Another First: Healthy Twins Born To Carriers Of Sickle Cell Disease - May
    http://www.cnn.com/HEALTH/9905/11/sickle.cell.success/index.html
    
    Extractions: Web posted at: 11:33 a.m. EDT (1533 GMT) NEW YORK (CNN) A New York-area couple who are both carriers of sickle cell disease have twin babies who are completely free of the sickle cell gene, thanks to a technique called pre-implantation genetic diagnosis (PGD), in which fertilized embryos are tested for the disorder before implantation in the woman's uterus. This first successful use of PGD to eliminate sickle cell disease was reported in Tuesday's Journal of the American Medical Association.

33. Sickle Cell Disease Review
    Promotes and disseminates research into the scientific, clinical and social aspects of this disorder. Literature review, bibliography, and general information on the disease.  
    http://scdreview.tripod.com/

34. Sickle Cell Disease In Children Familydoctor.org
    Information for parents about sickle cell disease in children from the American Academy of Family Physicians.  
    http://familydoctor.org/621.xml
    
    Extractions: Advanced Search familydoctor.org Home For Parents Special Conditions in Children Sickle Cell Disease in Children What is sickle cell disease? Who gets sickle cell disease, and how? What happens to red blood cells in sickle cell disease, and what problems can this cause? How can my doctor tell if my baby has sickle cell disease? ... Can sickle cell disease be cured? Printer-friendly version Email this article Sickle cell disease causes the red blood cells to make abnormal hemoglobin. Hemoglobin is the part of blood that carries oxygen in the body. There are different kinds of sickle cell disease. Some kinds are mild, but others cause serious illness. Return to top Sickle cell disease is most common in people whose ancestors came from Africa, Central America (especially Panama), South America, Caribbean nations, Mediterranean countries, India or Near Eastern countries. To get sickle cell disease, a child has to inherit the sickle hemoglobin gene from one parent and a sickle gene or another abnormal hemoglobin gene from the other parent. People with one normal gene and one sickle gene are carriers of the abnormal gene. This means that they have the sickle cell trait but not sickle cell disease. A child born to parents who both have sickle cell trait has a 25 percent chance of getting sickle cell disease.

35. Sickle Cell Disease: Information For School Personnel
    Information for school personnel.  
    http://www.state.nj.us/health/fhs/sicklecell/index.html
    
    Extractions: Special Child Health and Early Intervention Services Acknowledgements: The first edition Sickle Cell Disease: Management for the School Nurse was prepared by the Child Health Promotion, Pediatric Preventive Services, Health Promotion/Disease Prevention Services Unit and was adapted from Sickle Cell Disease: A Family Guide , New Jersey State Department of Health, 1993. This second edition was revised and edited by Richard A. Drachtman, M.D., Division of Pediatric Hematology/Oncology, University of Medicine and Dentistry of New Jersey/Robert Wood Johnson Medical School, in collaboration with the Sickle Cell Advisory Committee in New Jersey and the NJ Department of Health and Senior Services. This guide reflects the state of knowledge, current at the time of publication, on effective and appropriate care. Given the inevitable changes in the state of scientific information and technology, periodic review, update and revision will continue to be done. Funding for this edition was made available as part of a health services grant from Special Child, Adult and Early Intervention Services, Family Health Services, NJ Department of Health and Senior Services.

36. Sickle Cell Disease: Information For School Personnel
    The first edition sickle cell disease Management for the School Nurse was prepared Sickle Cell Advisory Committee. sickle cell disease Information for  
    http://www.state.nj.us/health/fhs/sicklecell/
    
    Extractions: Special Child Health and Early Intervention Services Acknowledgements: The first edition Sickle Cell Disease: Management for the School Nurse was prepared by the Child Health Promotion, Pediatric Preventive Services, Health Promotion/Disease Prevention Services Unit and was adapted from Sickle Cell Disease: A Family Guide , New Jersey State Department of Health, 1993. This second edition was revised and edited by Richard A. Drachtman, M.D., Division of Pediatric Hematology/Oncology, University of Medicine and Dentistry of New Jersey/Robert Wood Johnson Medical School, in collaboration with the Sickle Cell Advisory Committee in New Jersey and the NJ Department of Health and Senior Services. This guide reflects the state of knowledge, current at the time of publication, on effective and appropriate care. Given the inevitable changes in the state of scientific information and technology, periodic review, update and revision will continue to be done. Funding for this edition was made available as part of a health services grant from Special Child, Adult and Early Intervention Services, Family Health Services, NJ Department of Health and Senior Services.

37. Sickle Cell Disease: What Is It?
    Your Genes, Your Health, DNA Learning Center s multimedia guide to genetic, inherited disorders sickle cell, autosomal recessive, genetic disorder.  
    http://www.ygyh.org/sickle/whatisit.htm

38. Sickle Cell Disease - Your Genes, Your Health - DNA Learning Center - Cold Sprin
    Your Genes, Your Health, DNA Learning Center s multimedia guide to genetic, inherited disorders Fragile X syndrome, Marfan syndrome, Hemophilia,  
    http://www.ygyh.org/sickle/description.html
    
    Extractions: Fragile X Syndrome Sickle cell is one of the most common genetic disorders in the United States, affecting about 1 in every 375 African-American children. The painful crises, anemia, and organ damage of sickle cell can be traced back to the structure of an important blood protein called beta globin. Beta globin proteins are found inside red blood cells. The protein's job is to carry another molecule called heme. Inside the cells, beta and alpha globins combine to form hemoglobin, the molecule that delivers oxygen to all our cells. Two beta globins plus two alpha globins (and each globin's heme group) make one molecule of hemoglobin. The heme of each globin binds the oxygen molecule. The instructions for making beta globin are encoded inside a gene located on chromosome 11. Everybody has two chromosome 11s, so everyone has two beta globin genes. Inside the gene, code letters tell the cell’s protein-making machinery how to construct the protein. The machinery translates the code and puts the appropriate amino acids – the building blocks of proteins – into the proper positions. In people with sickle cell, the code inside both beta globin genes is different from usual. Instead of containing the letters G-A-G near the beginning of the gene, the code reads G-T-G. The usual G-A-G code tells the protein machine to put a glutamate amino acid into the protein, but the new G-T-G code tells the machine to put a valine in. The valine has a critical effect on the behavior of the entire hemoglobin molecule. When oxygen is released by the molecule, the valine becomes very sticky to the nearby V-shaped notch shown below. When two separate hemoglobins come near each other, the valine and notch interlock. More and more hemoglobins link up to the pair, and the structure explosively grows into a long rod of hemoglobins. (Because the rod is made up of interconnected hemoglobins, it is also known as a hemoglobin polymer.) The long polymers of hemoglobin are stiff and they stretch the red blood cell into the shape of a sickle, or a banana. The cell only springs back to its normal shape after it returns to the lung and captures more oxygen. Oxygen-binding instantly breaks up the polymers. As the red blood cells cycle through the body delivering oxygen, they repeatedly spring in and out of the sickle shape until the cells get stuck in the sickle shape. The stress of the shape changes also damages the cells, and the cells die after 10 to 20 days instead of living out their normal lifespan of 120 days. The premature death of the red bloods cells causes a shortage of red blood cells, a condition doctors call anemia. The shortage lowers the amount of oxygen delivered to the body’s tissues and causes the fatigue, shortness of breath, and the slow rate of growth seen in people with sickle cell disease. For reasons not completely understood, sickled cells and even normally-shaped cells are more likely to adhere to the walls of the blood vessels. The stiff sickled cells can’t squeeze past the blockage and they start piling up, creating a larger barrier that prevents even normally-shaped cells from passing by. With no red blood cells passing the obstruction, no oxygen can get to the tissues downstream, and cells in these tissues begin to die. This can cause very localized and severe pain in these tissues that can last hours, days, or even weeks. The blockages can occur anywhere in the body, but there are particular areas that are especially vulnerable. In the spleen, tissue damage impairs the ability of the spleen to filter bacteria out of the bloodstream and make antibodies to fight bacterial infections. Lungs can also be damaged by blocked vessels, a bacterial or viral infection, or fatty pieces of bone marrow that dislodge from the bone and get stuck in the lung. Red blood cells can’t pick up enough oxygen, and less oxygen causes more cells to sickle. The whole process can spiral into lung failure. Blockages in the brain’s blood vessels can cause a stroke if brain cells are killed. Usually, a person who has a stroke loses some ability to think; perceive sights, sounds, or smells; and walk or move easily. Most states in the U.S. screen for sickle cell disease at birth with a test called hemoglobin electrophoresis. This test uses a sample of blood from the infant and determines what types of hemoglobins are present. The final result looks something like this, where each different type of hemoglobin clusters into different dark spots in the electrophoresis gel. In this case, two different types of hemoglobin are present. The A-type is the normal type of hemoglobin, and the S-type is the sickle cell hemoglobin. Because this person makes both types, he carries one normal beta globin gene and one sickle beta globin gene. This makes him a carrier of sickle cell, but he does not have sickle cell disease. A person with sickle cell will have results like this, where only the S-type of hemoglobin is present. This person also has two genes for beta globin, but both make the same sickle cell version. Finally, a person who does not have sickle cell and does not carry the sickle cell gene will only make the A-type of hemoglobin. Both of his beta globin genes produce the non-sickling version of the protein. The different results in this test occur because the A-type form of hemoglobin has a different mobility than the S-type form. The A-type moves quickly through a slab of gel, while the S-type moves more slowly. If the two forms are propelled through a gel for the same amount of time, they will separate into distinct bands in different parts of the gel. If two bands are present, then the person being tested has both forms of hemoglobin. He or she is a carrier for the sickle cell disease. If the person being tested has the disease, he or she will have two copies of the S-type of hemoglobin, and only one band will appear on the gel. If the person being tested has the disease, he or she will have two copies of the S-type of hemoglobin, and only one band will appear on the gel. If the person being tested does not have the disease (and is not a carrier), only one band will appear on the gel, that of the A-type hemoglobin. One blood test can distinguish the difference between people with and without sickle cell, and people who are carriers of sickle cell. Sickle cell disease can also be detected in the unborn fetus or in an embryo conceived in a test tube. In these cases, the test looks directly into the genes of the fetus or embryo, and a DNA fingerprint of the beta globin genes is constructed. When the test is complete, the pattern on the DNA fingerprint reveals whether the embryo does or does not have sickle cell disease, or is a carrier. The first step in making the fingerprints is isolating the embryo's two beta globin genes, and copying them millions of times with a chemical reaction called polymerase chain reaction (PCR). When enough copies of the genes are made, a special enzyme is added to the mixture. The enzyme cuts A-type DNA pieces in two, but leaves the S-type untouched. Therefore, an embryo with both A- and S-type genes will produce three different groups of DNA fragments: the two small pieces from the A-type gene and the larger, untouched, S-type gene. The final step in the test is to visualize the DNA pieces generated through a process called gel electrophoresis. The process sorts each group of pieces into a unique position inside a hard slab of gel. A pattern with three spots indicates the embryo does not have sickle cell disease but is a carrier. A pattern with one spot indicates the embryo has sickle cell. A pattern with two spots indicates that the embryo does not have the sickle cell disease. A pattern with three spots means the embryo is a carrier; one spot means the embryo has sickle cell disease, and two spots means the embryo does not have the disease. Sickle cell anemia is an inherited disorder and is not contagious. A person gets sickle cell when he inherits an S-type beta globin gene from each parent. Each parent has two beta globin genes: one is the "normal" A-type, and the other is the sickling S-type (represented by the red chromosome). When the father and mother produce sperm and eggs, only one of their two beta globin genes enter each cell. About half the cells get the S-type gene, while the others get the A-type gene. When a sperm (from the father) carrying the S gene fertilizes an egg (from the mother) carrying the S gene, the resulting child inherits both genes and develops sickle cell anemia. Inheritance begins with the parents, and like all people, each parent has two beta globin genes, as represented by the chromosome pairs below. Both have one "normal" A-type (grey chromosomes), but the father also has a C (blue chromosome), while the mother has an S (red chromosome). When the father and mother produce sperm and eggs, only one of their two beta globin genes enter each cell. About half of the father's sperm get the A-type gene, while the other half get the C-type gene. Similarly, half the mother's eggs get the A-type gene, the other half get the S-type gene. When a sperm carrying the C-type gene fertilizes an egg carrying the S-type gene, the resulting child will inherit both genes and develop SC disease. The symptoms of SC disease are generally milder than sickle cell anemia (SS). A person gets Sß when she inherits an S-type beta globin gene from one parent and a ß-type beta globin gene from the other. (ß genes produce little or no beta globin). Inheritance begins with the parents, and like all people, each parent has two beta globin genes, as represented by the chromosome pairs below. Both have one "normal" A-type (grey chromosomes), but the father also has a ß (purple chromosome), while the mother has an S (red chromosome). When the father and mother produce sperm and eggs, only one of their two beta globin genes enter each cell. About half the cells get the A-type gene, while half the sperm get the b-type gene, and half the eggs get the S-type gene. When a sperm carrying the b-type gene fertilizes an egg carrying the S-type gene, the resulting child will inherit both genes and develop the sickling Sb disease. The severity of Sb depends on the specific variant of b inherited. When both parents carry an S gene, every child they have has a 1-in-4 chance of inheriting sickle cell anemia. To see why, we'll construct a Punnett square. First, we place the parents' genes on the outside of the square, as shown in the animation. Each box inside the Punnett square represents a possible child of this couple. To complete the boxes, we move one gene from each parent into every box, as shown below. Now we inspect the boxes for the pair of genes that causes sickle cell anemia (SS). Out of four boxes, only one contains the SS pair, so each child of this couple has a 1-in-4 (25%) chance of getting sickle cell anemia. The most important thing to remember about these odds is that they apply to every child this couple has. It may be useful to think of the Punnett square as a roulette wheel. Each child is a separate "spin of the wheel," so each child has a 25% chance of developing sickle cell. In this family, one in four children has sickle cell disease. Other couples with the mutation may have two, three, four, or even no children with the disease. When one parent carries a C-type gene and the other carries an S-type, every child they have has a 1-in-4 chance of inheriting SC disease. To see why, we'll construct a Punnett square. First, we place the parents' genes on the outside of the square, as shown in the animation. Each box inside the Punnett square represents a possible child of this couple. To complete the boxes, we move one gene from each parent into every box, as shown below. Now we inspect the boxes for the pair of genes that causes SC disease (SC). Out of four boxes, only one contains the SC pair, so each child of this couple has a 1-in-4 (25%) chance of getting SC. The most important thing to remember about these odds is that they apply to every child this couple has. It may be useful to think of the Punnett square as a roulette wheel. Each child is a separate "spin of the wheel," so each child has a 25% chance of developing SC disease. In this family, one in four children has sickle cell disorder. Other couples with the mutation may have two, three, four, or even no children with the disorder. When one parent carries a b-type gene and the other carries an S-type, every child they have has a 1-in-4 chance of inheriting Sb disease. To see why, we'll construct a Punnett square. First, we place the parents' genes on the outside of the square, as shown in the animation. Each box inside the Punnett square represents a possible child of this couple. To complete the boxes, we move one gene from each parent into every box, as shown below. Now we inspect the boxes for the pair of genes that causes Sb disease (Sb). Out of four boxes, only one contains the Sb pair, so each child of this couple has a 1-in-4 (25%) chance of getting the sickling Sb disease. The most important thing to remember about these odds is that they apply to every child this couple has. It may be useful to think of the Punnett square as a roulette wheel. Each child is a separate "spin of the wheel," so each child has a 25% chance of developing Sb disease. In this family, one in four children has sickle cell disorder. Other couples with the mutation may have two, three, four, or even no children with the disorder. Sickle cell disease is common in many regions of the world where mosquito-borne malaria is present. It is believed that people who carry only one sickle cell mutation (they do not have the disease) can tolerate malaria better than people who carry no mutations. This may be why the mutation persists in the population despite the high mortality associated with untreated sickle cell disease. Pain associated with blocked blood vessels is the most obvious symptom, and can be severe enough to warrant hospitalization. The blocked blood vessels frequently lead to spleen, lung, and heart damage and stroke. Sickle cell also causes anemia, which leads to fatigue. Sickle cell disease is the most common single gene disorder in African-Americans, affecting one in every 375. Globally, a quarter of a million children are born with the disease each year, mainly in Africa, the Mediterranean, Arabia, and South Asia. In most states, newborns are screened for hemoglobin disorders, including sickle cell. The screening test determines which hemoglobin types each child makes. A child with sickle cell makes hemoglobin S instead of the usual hemoglobin A. Sickle cell diseases include three distinct types: sickle cell anemia, SC disease, and Sb disease. They are caused by a mutation in a blood protein called beta globin. The mutation leads to changes in the shape and behavior of red blood cells. The sickled, stiff, and sticky red blood cells of sickle cell disease cause severe organ damage and intense pain. A bone marrow transplant is the only available cure, but it is a high risk operation. Although it has been successful in severely affected children, adults have a tendency to reject the transplant. The drug hydroxyurea helps to prevent or lessen sickle cell's complications; blood transfusions and narcotics for pain also help to alleviate the symptoms. Facts and Theories Symptoms Incidence Testing and Screening Cause Treatment. How is sickle cell treated? Acute Chest Syndrome Dr. Kusm Viswanathan talks about the danger of ACS as one major complication resulting from sickle cell. She discusses ACS treatment options for children and adults. Pain Dr. Viswanathan talks about the cause of pain associated with sickle cell and how it can be treated. Strokes Dr. Viswanathan talks about the dangers of strokes in children with sickle cell. She describes the transcranial Doppler imaging that can help detect potential stroke victims. Heart Problems Dr. Viswanathan talks about the need to monitor heart function in people with sickle cell. Kidneys and Gallbladders Dr. Viswanathan talks about kidney and gallbladder problems that people with sickle cell may have to deal with. Retinopathy Dr. Viswanathan talks about retinopathy, a condition associated with sickle cell that can cause blindness. However, with early detection and treatment, blindness can be prevented. What is it like to have sickle cell? School Maya Priest talks about how sickle cell affected her ability to attend school, and how she had to work with tutors in order to keep up with her schoolwork. Dealing with the Pain Maya discusses the different levels of tolerance and how she deals with the pain. Skepticism Maya talks about the skeptical attitudes of some doctors and nurses; they can’t “see” the pain, so it must not be real. She also talks about her friend who died, partially because of these dangerous attitudes. Complications Maya talks about some of the physical complications that she may have to deal with as she gets older. Job complications Maya discusses the difficulty of securing a normal job because of her unpredictable illness. Having Fun Maya talks about the importance of having fun despite the risk of getting sick. Setting Limits Maya talks about the importance of setting limits and how the limits can vary for different people. Having Children Maya discusses her desire to have children and the health risks she faces if she becomes pregnant. Relationships Maya talks about her relationships with other people and the possibility of finding a partner who can understand and deal with the complications of her condition. Advice to Parents Maya gives parents some advice: education and support. Alzheimer Disease

39. Sickle Cell Foundation Of Alberta - Home
    Educates the public about sickle cell disease and provides support for carriers of the trait and their families.  
    http://www.sicklecellfoundationofalberta.org
    
    Extractions: The Sickle Cell Foundation of Alberta was founded as a private non-profit organization to educate the public about Sickle Cell Disease and to provide support for carriers of the trait and their families. The foundation aims to provide quality education and promote public professional awareness about sickle cell disease

40. EMedicine - Pediatrics, Sickle Cell Disease : Article By Nedra Dodds, MD
    Pediatrics, sickle cell disease sickle cell disease is an inherited disorder of hemoglobin synthesis. The resulting abnormality produces a normocytic,  
    http://www.emedicine.com/emerg/topic406.htm
    
    Extractions: (advertisement) Home Specialties Resource Centers CME ... Patient Education Articles Images CME Advanced Search Consumer Health Link to this site Back to: eMedicine Specialties Emergency Medicine Pediatric Last Updated: June 13, 2005 Rate this Article Email to a Colleague Synonyms and related keywords: sickle cell anemia, sickle disease, sickle hemoglobinopathy syndromes, hemolytic anemia, aplastic anemia crisis, hemoglobin synthesis, sickle cells, homozygous sickle cell disease AUTHOR INFORMATION Section 1 of 9 Author Information Introduction Clinical Differentials ... Bibliography Author: Nedra Dodds, MD , Consulting Staff, Department of Emergency Medicine, Tanner Medical Center Coauthor(s): Hosseinali Shahidi, MD, MPH , Assistant Professor, Departments of Emergency Medicine and Pediatrics, State University of New York and Health Science Center at Brooklyn Nedra Dodds, MD, is a member of the following medical societies: American College of Emergency Physicians American Medical Association , and National Medical Association Editor(s): Garry Wilkes, MD

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