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Sickle Cell Anemia:     more books (100)

A child with sickle cell anemia in your class: (a guide for teachers) by Roland B Scott, 1977 Dying in the City of the Blues: Sickle Cell Anemia and the Politics of Race and by Keith Wailoo, 2001-01-01 The Official Patient's Sourcebook on Sickle Cell Anemia: Directory for the Internet Age by Icon Health Publications, 1980 Sickle cell anemia (SuDoc HE 20.3031:Si 1) by U.S. Dept of Health and Human Services, 1990 Sickle Cell Anemia Sickle cell anemia: Diagnosis, pathology, complications, and therapy : January 1969 through April 1972 : 339 citations (Literature search / National Library of Medicine) by Charlotte Kenton, 1972 Sickle cell anemia and genetic counseling (Working paper) by Jack R Meredith, 1973 Sickle cell anemia research in Memphis: Interview with Alfred P. Kraus, M.D., October 27, 1989 by Frankie L Winchester, 1989 Tanya's Daddy: A Story About Sickle-Cell Anemia by Peter Anderson, Myra Anderson, et all 1995-05 Sickle cell anemia (LC science tracer bullet) by Leroy D Davis, 1982 Depression and ego integration manifested in drawings of adolescents with sickle cell anemia: A pilot study by Kathryn D'Arcy Lyness, 1979 Sickle cell anemia: Implications for newborn screening : a self learning module for nurses by Ellie Mulcahy, 1993 Sickle cell anemia: Counselor's handbook by Robert P Locey, 1972 Amendments to revise programs for sickle cell anemia and other genetic disorders, 1975 by United States. Congress. Senate. Committee on Labor and Public Welfare. Subcommittee on Health., 1975-01-01

lists with details

101. MSN Encarta - Sickle-Cell Anemia
     Search for books and more related to sicklecell anemia sickle-cell anemia is caused by a defective gene that produces an abnormal form of hemoglobin,  
     http://encarta.msn.com/encyclopedia_761577849/Sickle-Cell_Anemia.html
     
     Extractions: Web Search: Encarta Home ... Upgrade your Encarta Experience Search Encarta Upgrade your Encarta Experience Spend less time searching and more time learning. Learn more Tasks Related Items more... Further Reading Search for books and more related to Sickle-Cell Anemia Encarta Search Search Encarta about Sickle-Cell Anemia Advertisement document.write(' Encyclopedia Article Multimedia 3 items Sickle-Cell Anemia genetic disorder of the blood leading to frequent and severe infections, damage to major organs, and episodes of unpredictable pain in the back, chest, abdomen, and extremities. Early symptoms appear at about six months of age and may include serious infections, pain and swelling in the hands and feet, and enlargement of the abdomen and heart. According to the National Institutes of Health, this disease affects 72,000 people in the United States, primarily African Americans. Sickle-cell anemia is caused by a defective gene that produces an abnormal form of hemoglobin , the component of red blood cells responsible for transporting oxygen from the lungs to the tissues. The abnormal hemoglobin, called hemoglobin S, distorts red blood cells after they release oxygen in the tissues. These distorted cells are called sickled cells because of their resemblance to the sickle, a type of crescent-shaped cutting blade used in agriculture. The sickled shape makes it difficult for these cells to pass through tiny blood vessels, resulting in intensely painful blockages that prevent vital oxygen and nutrients in the blood from reaching organs and tissues, impairing their function. As a result, sickle-cell patients are also vulnerable to a number of infections. When the blood flow to the brain is affected, sickle-cell patients may experience brain damage, such as

102. Sickle Cell Disease
     Thanks to advancements in early diagnosis and treatment, most children born with this disorder grow up to live relatively healthy and productive lives.  
     http://kidshealth.org/parent/medical/heart/sickle_cell_anemia.html
     
     Extractions: Sickle cell disease is an inherited disorder of the red blood cells characterized by abnormally shaped red cells. This abnormality can result in painful episodes, serious infections, chronic anemia, and damage to body organs. These effects can, however, vary from person to person depending on the type of sickle cell disease the person has. Some individuals are relatively healthy and others are hospitalized frequently. But thanks to advancements in early diagnosis and treatment, most children born with this disorder grow up to live relatively healthy and productive lives. A Closer Look at Sickle Cell Disease The different forms of sickle cell disease are determined by the genes that are inherited from the person's parents. An individual has the disease if he or she inherits a sickle cell gene from each parent ( hemoglobin SS disease , also called sickle cell anemia He or she can also inherit a sickle cell gene from one parent and a different kind of abnormal gene from the other and end up with a different form of sickle cell disease, such as hemoglobin SC disease and hemoglobin S-thalassemia If an individual inherits only one sickle cell gene and a normal gene from the other parent, then he or she will have the sickle cell trait, but not the disease. A blood

103. Sickle Cell Information Center Home Page
     The Mission of the sickle cell Information Center www.SCInfo.org. The mission of this site is to provide sickle cell patient and professional education,  
     http://www.scinfo.org/

104. Sickle Cell Disease
     Care Coordination for Patients with sickle cell Disease Gall Bladder and Liver Disorders in sickle cell Disease a Critical Review  
     http://sickle.bwh.harvard.edu/menu_sickle.html

105. Information Center For Sickle Cell And Thalassemic Disorders
     Gives an evaluation of the causes and treatments of sickle cell disease as well as current research. Information is available both for lay persons as well  
     http://sickle.bwh.harvard.edu/

106. Sickle Cell Disease Association Of America -- SCDAA Home
     the sickle cell Disease Awareness Commemorative stamp on Thursday evening, Sept. 25, at the 31st annual convention of sickle cell Disease Association of  
     http://www.sicklecelldisease.org/
     
     Extractions: A word from SCDAA on Hurricane Katrina The President, Chairman, National Board of Directors and staff of Sickle Cell Disease Association of America, Inc., express their heartfelt sympathies and concerns to all those affected by the recent devastation caused by hurricane Katrina. President's Corner Statement from Dr. Willarda V. Edwards Stamp of Approval National Spokesperson SEPTEMBER IS NATIONAL SICKLE CELL DISEASE AWARENESS MONTH! Our SCDAA family has many activities planned . Please click here for more information Fri., Sept. 30 at Univ. of Texas at Dallas Seminar "Lentivirus-Mediated Gene Therapy of Sickle Cell Disease" Please click here for more information The U.S. Postal Service unveiled the Sickle Cell Disease Awareness Commemorative stamp on Thursday evening, Sept. 25, at the 31st annual convention of Sickle Cell Disease Association of America Inc.. Click here to purchase SCDAA National Stamp products.

107. 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

108. 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

109. Genome.gov | Learning About Sickle Cell Disease
     Answers to frequently asked questions about sickle cell disease, published by the National Human Genome Research Institute.  
     http://www.genome.gov/10001219
     
     Extractions: triggerParms["cpp_5"] = "Referer:"+ cppUrlPatch (""); // Optional Home About NHGRI Newsroom Staff ... Specific Genetic Disorders Learning About Sickle Cell Disease What do we know about heredity and sickle cell disease? Is there a test for sickle cell disease? NHGRI Clinical Research on Sickle Cell Disease Additional Resources for Sickle Cell Disease Information Sickle cell disease is the most common inherited blood disorder in the United States. Approximately 80,000 Americans have the disease. In the United States, sickle cell disease is most prevalent among African Americans. About one in 12 African Americans and about one in 100 Hispanic Americans carry the sickle cell trait, which means they are carriers of the disease. Sickle cell disease is caused by a mutation in the hemoglobin-Beta gene found on chromosome 11. Hemoglobin transports oxygen from the lungs to other parts of the body. Red blood cells with normal hemoglobin (hemoglobin-A) are smooth and round and glide through blood vessels. In people with sickle cell disease, abnormal hemoglobin molecules - hemoglobin S - stick to one another and form long, rod-like structures. These structures cause red blood cells to become stiff, assuming a sickle shape. Their shape causes these red blood cells to pile up, causing blockages and damaging vital organs and tissue.

110. Genomics|HuGENet|Reviews|Hb S Allele And Sickle Cell Disease
     The mission of the Office of Genomics and Disease Prevention is to integrate advances in human genetics into public health research, policy, and programs.  
     http://www.cdc.gov/genomics/hugenet/reviews/sickle.htm
     
     Extractions: Abstract Gene Gene Variants Disease ... Medical Literature Search ABSTRACT Beta globin is a major component of adult hemoglobin. The gene for beta globin is located on chromosome 11 and there are over 475 allelic variants. One of these variants, sickle hemoglobin ( Hb S ), is responsible for sickle cell disease, one of the most prevalent genetic diseases, affecting over 50,000 Americans. Most individuals with sickle cell disease have African and Mediterranean ancestry. It is believed that the high frequency of the ( Hb S ) variant is maintained in these populations by the increased resistance to malaria infection in heterozygous carriers, those individuals who possess one copy of the normal beta globin gene (Hb A) and one copy of the sickle variant (

111. Sickle Cell Disease Practical Tips For Preventing A Sickle Cell
     Information about preventing a sickle cell crisis from the American Academy of Family Physicians.  
     http://familydoctor.org/550.xml
     
     Extractions: Advanced Search familydoctor.org Home Conditions A to Z Preventing a Sickle Cell Crisis What is sickle cell disease? What is a sickle cell crisis? What causes a sickle cell crisis? What medicines can I use at home to control my pain? ... What else can I do to control the pain? Printer-friendly version Email this article Sickle cell disease, also called sickle cell anemia, is a hereditary (you inherit it from your parents) problem that causes a type of faulty hemoglobin in red blood cells. Hemoglobin carries oxygen in the blood. Normal red blood cells are disc-shaped and very flexible. In sickle cell disease, some red blood cells can change shape so that they look like sickles or crescent moons. Because of their shape, they don't move well through the smallest blood vessels. This can stop or slow blood flow to parts of the body, causing less oxygen to reach these areas. The sickle cells also die earlier than normal blood cells, which can cause a shortage of red blood cells in the body. There is no cure for sickle cell disease. Return to top What is a sickle cell crisis?

112. Sickle Cell Disease: Information For School Personnel
     The first edition sickle cell Disease Management for the School Nurse was prepared by the Child Health Promotion, Pediatric Preventive Services,  
     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.

113. Sickle Cell Disease Association Of The Piedmont
     A sickle cell Disease and HIV AIDS agency in Greensboro, North Carolina.  
     http://www.scdap.org/
     
     Extractions: QUICK VIEW - SITE PAGES Click HERE for Job Opportunities Mission Statement Sickle Cell Page HIV/AIDS Page AIDS Research ... Wake Forest Center PLEASE VISIT OUR SPECIAL CORPORATE PARTNER POLO RALPH LAUREN FOR MEN, WOMEN AND CHILDREN'S STYLES > click on logo Sickle Cell Disease Association of the Piedmont ATTENTION! If you cannot see our introductory page then your computer did not come with Flash 5 Player installed. It takes less than a minute to install and you will need it in the future as you surf the WEB. Click HERE to install it and then come back to our page. OR Click HERE to visit all our other site pages.

114. Sickle Cell Disease In Childhood: Part II. Diagnosis And Treatment Of Major Comp
     Complications of sickle cell disease occur suddenly and can rapidly become severe. A child with sickle cell disease who is acutely ill is usually best  
     http://www.aafp.org/afp/20000915/1309.html
     
     Extractions: AAFP Home Page Journals Vol. 62/No. 6 (September 15, 2000) Treatment advances over the past 25 years have significantly decreased morbidity and mortality in children with sickle cell disease. Aggressive management of fever, early diagnosis of acute chest syndrome, judicious use of transfusions and proper treatment of pain can improve quality of life and prognosis for these children. Prophylactic hydroxyurea therapy has been shown to reduce the incidence and severity of pain crises in adults with sickle cell disease and has been effective in limited studies conducted in children. Research into stem cell transplantation provides hope that a cure for sickle cell disease may be possible. (Am Fam Physician 2000;62:1309-14.) C omplications of sickle cell disease occur suddenly and can rapidly become severe. Infection, acute splenic sequestration crisis, aplastic crisis, acute chest syndrome, stroke, cholelithiasis, renal disease and pain are the major complications of this disease in children. Some complications lend themselves to simple management, whereas others, including aseptic necrosis of the hip, priapism and leg ulcers, require prompt referral for specialized treatment Table 1 ). A child with sickle cell disease who is acutely ill is usually best managed in a facility that can provide pediatric tertiary care.

115. Noah.cuny.edu/pregnancy/march_of_dimes/birth_defec
     sickle cell Disease disease informationHealth information discussing sickle cell disease, which is a hereditary blood disorder that affects the red blood cell.  
     http://noah.cuny.edu/pregnancy/march_of_dimes/birth_defects/siklcell.html

116. Sickle Cell Disease
     sickle cell disease is a genetic blood disorder that affects the hemoglobin within the red blood cells.  
     http://www.stjude.org/disease-summaries/0,2557,449_2162_2955,00.html
     
     Extractions: @import url(/StJude/CDA/Common/CSS/default.css); @import url(/StJude/CDA/Common/CSS/default_lists.css); @import url(/StJude/CDA/Common/CSS/default_content_types.css); @import url(/StJude/Common/CSS/St_Jude_Clinical_Science); The following browsers support numerous web standards including CSS, XHTML, and the DOM (a universal means of controlling the behavior of web pages): St. Jude Children's Research Hospital Home Clinical Science Home Disease Information Hematologic Disorders Related Topics Sickle Cell Disease Parent Information Transfusions reduce ACS in sickle cell patients Sickle cell may delay brain growth Symposiums at St. Jude

117. Sickle Cell Sufferers Living Longer, Dying Less
     University of Texas Southwestern Medical Center at Dallas.  
     http://www8.utsouthwestern.edu/utsw/cda/dept37389/files/158834.html
     
     Extractions: from their disease Latest News More Medical News Video News Releases En Espanol ... Publications Staff DALLAS - March 25, 2004 - Children with sickle cell disease - an inherited red blood-cell disorder - are living longer, dying less often from their disease and contracting fewer fatal infections than ever before, researchers at UT Southwestern Medical Center at Dallas report. Their study, which will appear in the June edition of the scientific journal Blood In one of the largest published sickle cell studies to date, UT Southwestern researchers, including Dr. Charles Quinn (left), assistant professor of pediatrics and Dr. Zora Rogers, associate professor of pediatrics, discovered that children with sickle cell disease today have a 12 percent increase of survival at 18 years of age from comparable statistics of 30 years ago. Thirty years ago, only half of children with sickle cell disease were expected to reach adulthood. This new study showed that patients with sickle cell anemia, the severest and most common form of the disease, had a survival rate of 85.6 percent at 18 years old, and patients with milder forms of sickle cell disease had a survival rate of 97.4 percent at 18. Also, 11.5 percent of patients with sickle cell anemia had a stroke by 18 years old. Although this rate remains constant, fewer children are dying as a result of the stroke, researchers said.

118. Sickle Cell Disease Definition - Medical Dictionary Definitions Of Popular Medic
     Online Medical Dictionary and glossary with medical definitions.  
     http://www.medterms.com/script/main/art.asp?articlekey=9368

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