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Draad: Drepanositose (en hoekom dit belangrik is)

  1. #1
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    Verstek Drepanositose (en hoekom dit belangrik is)



    According to medical experts, Sickle-Cell Disease, or Sickle-Cell Anaemia (SCD or SCA) or drepanocytosis, is a genetic blood disorder characterised by red blood cells that assume an abnormal, rigid, sickle shape. Sickling decreases the cellsí flexibility and results in a risk of various complications. The sickling occurs because of a mutation in the haemoglobin gene.

    The term Ďdiseaseí is applied because the inherited abnormality causes a pathological condition that can lead to death and severe complications. Indeed, in sickle cell, life expectancy is shortened, with studies reporting an average life expectancy of 42 in males and 48 in females.

    Sickle cell anaemia is a serious disease in which the body makes sickle-shaped red blood cells. In other words, the red blood cells are shaped like a ďC,Ē while the normal red blood cells are disc-shaped and look like doughnuts without holes in the centre.

    Normal blood cells move easily through the blood vessels. Red blood cells contain the protein hemoglobin. This iron-rich protein gives blood its red color and carries oxygen from the lungs to the rest of the body.

    On the other hand, sickle cells contain abnormal hemoglobin that causes the cells to have a sickle shape. Sickle-shaped cells donít move easily through the blood vessels; they are stiff and sticky and tend to form clumps and get stuck in the blood vessels.

    The clumps of sickle cells block blood flow in the blood vessels that lead to the limbs and organs. Blocked blood vessels can cause pain, serious infections and organ damage.

    Sickle cell anaemia is one type of anaemia, which is a condition in which the blood has a lower than normal number of red blood cells. This condition also can occur if the red blood cells donít have enough hemoglobin.

    Red blood cells are made in the spongy marrow inside the large bones of the body. Bone marrow is always making new red blood cells to replace old ones. Normal red blood cells last about 120 days in the bloodstream and then die. They carry oxygen and remove carbon dioxide (a waste product) from the body.

    In sickle cell anaemia, a lower-than-normal number of red blood cells occurs because sickle cells donít last very long. Sickle cells usually die after only about 10 to 20 days. The bone marrow canít make new red blood cells fast enough to replace the dying ones, hence the crises usually experienced by sufferers.

    Sickle cell anaemia is an inherited, lifelong disease. People who have the disease are born with it. They inherit two copies of the sickle cell geneóone from each parent.

    People who inherit a sickle cell gene from one parent and a normal gene from the other parent have a condition called sickle cell trait, which is different from sickle cell anaemia. People who have sickle cell trait donít have the disease, but they have one of the genes that cause it. Like people who have sickle cell anaemia, people who have sickle cell trait can pass the gene to their children.

    According to the chairman of the Sickle Cell Foundation Nigeria, Prof. Olu Akinyanju, over 40 million Nigerians are carriers of the sickle cell gene. And as frightening as it is, statistics say, about 150,000 babies are born yearly with the sickle cell anaemia.
    http://www.punchng.com/Articl.aspx?t...01006090504510
    Kan julle al sien wat die antwoord is?

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    Verstek Ant: Drepanositose (en hoekom dit belangrik is)

    Hier is die antwoord:
    Sickle cell disease anemia

    n.
    A chronic, usually fatal anemia marked by sickle-shaped red blood cells, occurring almost exclusively in Black people of Africa or of African descent, and characterized by episodic pain in the joints, fever, leg ulcers, and jaundice. The disease occurs in individuals who are homozygous for a mutant hemoglobin gene. Also called sickle cell disease.

    http://www.answers.com/topic/sickle-cell-anemia

  3. #3
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    Verstek Ant: Drepanositose (en hoekom dit belangrik is)

    EN nou weier die Negroides om getoets te word daarvoor. Hulle sal eerder doodgaan.
    Sickle cell testing of athletes stirs discrimination fears


    Among the NCAA football players who have died over the past decade from overexertion on the field are (clockwise from top left) Preston Birdsong, Dale Lloyd, Aaron Richardson, and Ereck Plancher. (AP

    By Rob Stein
    Washington Post Staff Writer
    Monday, September 20, 2010; 12:19 AM


    U.S. colleges and universities for the first time are requiring top student athletes to submit to testing for the gene for sickle cell anemia, a mandate aimed at preventing sudden deaths of promising young players but stirring deep fears about reviving dangerous old prejudices.

    The screening hopes to identify athletes at high risk for life-threatening complications from intense physical exertion. That way, those with the gene could be monitored more closely and their training could be modified by, for example, allowing more time for rest and drinking more water.

    But the prerequisite is evoking some of the most notorious episodes in the nation's history. While less known than the infamous Tuskegee syphilis experiment, for decades blacks were stigmatized by sickle cell because they carried it far more commonly than whites, marking them as supposedly genetically inferior, barring them from jobs, the military, insurance and even discouraging them from marrying and having children.

    "This amounts to a massive genetic screening program, with tens of thousands being screened," said Troy Duster, a professor of sociology at New York University who studies the racial implications of science. "This could have an extraordinarily heavy impact on black athletes. You are going to be picking out these kids and saying, 'You are going to be scrutinized more closely than anyone else.' That's worrisome."

    The testing is being watched closely as a case study in both the potential benefits and risks of large-scale modern genetic screening, which is proliferating as the genetic bases for more and more diseases are being deciphered.

    "This could be a tip of an iceberg of genetic screening as we go forward," said Vence L. Bonham of the National Institutes of Health's National Human Genome Research Institute. "Getting it right is important, especially this one being the first one out of the gate."

    Although endorsed by some doctors, sports officials, athletes and parents, the testing has raised objections from both the Sickle Cell Anemia Association of America and a federal panel that advises the government on issues related to genetic testing.

    "We're very concerned that identifying someone as a carrier could be discriminatory," said R. Rodney Howell, who chairs the Health and Human Services Department's Advisory Committee on Heritable Disorders in Newborns and Children, which sent a letter to HHS Secretary Kathleen Sebelius in June expressing concern about the program. "There is no need to single out this group."

    The National Collegiate Athletic Association mandated the testing in April in response to a lawsuit filed by the family of Dale Lloyd II, a 19-year-old African American freshman at Rice University who died after an intense football workout in 2006 and was later discovered to have had the sickle cell trait.

    "We want to prevent this from happening to anyone else," said Lloyd's mother, Bridgette Lloyd of Houston. "Coaches and trainers need this knowledge. We don't want another young person to lose their life because of a lack of information."

    Under the policy, as of Aug. 1 all new students joining NCAA Division I teams, regardless of race, must be tested for the sickle cell trait - a requirement affecting about 170,000 student-athletes. No one will be excluded from sports or restricted in training or playing based on the results, officials said. Rather, athletes who test positive will be conditioned more carefully and watched more closely to ensure they drink enough and avoid overexertion, especially on hot days and in high altitudes. The NCAA is considering expanding the testing to Division II and III players, which would extend the order to about 260,000 more students.

    "We're trying to protect the health and well-being of our student athletes," said Yvette Rooks, the University of Maryland's team physician, who served on the NCAA committee that recommended the policy. "One death is too many. Anything we can do to prevent it and help people be healthier is important."

    Sickle cell anemia creates sickle-shaped red blood cells, which block vessels, causing chronic problems with intense pain, life-threatening infections and organ damage.

    A person born with two copies of the gene gets the illness. People who carry only one - known as having the sickle cell trait - are generally healthy. But during highly stressful physical exertion their blood cells can become sickle-shaped, preventing the delivery of oxygen to tissues and organs. Since 2000, as many as 10 Division I college football players who had the trait without knowing it have died suddenly following workouts.

    "There have been players who cease activity on a hot day because of complaints of fatigue - they are sweating heavily and cramping and not understanding the evidence of sickling. Those cases have been managed as exertional heat illness - and it wasn't, with tragic consequences," said Scott A. Anderson, head athletic trainer at the University of Oklahoma, who has spearheaded the drive for testing. "The more you know, the better the athlete can protect themselves."

    Students can opt out if they prove that they have already been tested or sign a waiver insulating their school from liability, though the NCAA is considering revoking that option. Even if students can refuse, critics worry that they will fear antagonizing coaches or other athletic officials, putting their scholarships and possible future professional careers in jeopardy. Coaches may be hesitant to intensively train and play those who test positive, and professional teams may be less inclined to draft them.

    "The stigma and its consequences - both self-imposed and done by coaches, peers, and the institution - are likely to be far, far out of proportion to the actual risk," said Duster, who chaired the Human Genome Project's National Advisory Committee on Ethical, Legal and Social Implications.

    While acknowledging that the trait may carry some risk, critics of the new policy also say the magnitude remains far from clear. Many athletes with the trait play safely in extreme conditions. And athletes who do not carry the gene have suddenly died for other reasons, most notably heart problems.

    "What doesn't exist is scientific data to support the screening," said Elliott Vichinsky, director of hematology-oncology at Children's Hospital in Oakland and director of the Northern California Sickle Cell Center. "There are a lot of other people at risk for heat-related illness from exertion."

    The best solution, they argue, would be better monitoring, training and care for all athletes - a strategy that worked for the military. That would avoid targeting the estimated 8 percent of blacks who carry the sickle cell trait gene, compared with about 0.2 percent of whites and 0.5 percent of Hispanics. In 2008-09, 24.8 percent of male Division I student-athletes and 16 percent of female Division I student-athletes were black, according to NCAA statistics.

    "If you want to protect people, there's an easy way to do that: change the training protocol for everyone," said Lanetta Jordan, the Sickle Cell Disease Association of America's chief medical officer.

    In addition, critics worry that students who test positive for the trait and their families will misinterpret the results as meaning they have sickle cell anemia, particularly if the news is not delivered by a doctor or genetic counselor.

    "If you are going to test for sickle cell trait, it should not be done in the locker room by a coach," Howell said.

    But supporters argue that such concerns are easily outweighed by the benefits.

    "There have been no known case of any athletes being denied participation in sport because of their sickle trait status," Anderson said. "Information beats ignorance."

    Others, while raising questions about the testing, hesitate to condemn the program as ill-conceived.

    "I see it as an experiment," said Lawrence C. Brody, also of the National Human Genome Research Institute. "It's an opportunity for us to learn."
    http://www.washingtonpost.com/wp-dyn...091904417.html
    Last edited by Rooi Jan; 24 Sep 2010 at 09:59.

  4. #4
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    Verstek Ant: Drepanositose (en hoekom dit belangrik is)

    Ek neem aan saam met die hiv is hierdie n dodelike kombinasie.

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    Verstek Ant: Drepanositose (en hoekom dit belangrik is)

    Dit lyk nie so as 'n mens na die draers van die siekte se getalle kyk nie....

  6. #6
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    Verstek Ant: Drepanositose (en hoekom dit belangrik is)

    Mense wat sekelsiekte het kan nie malaria kry nie... hierdie genetiese toestand het ontplof aangesien dit die enigste mense is wat nie in miljoene gesterf het aan malaria nie. Dus, die enigste mense wat oud genoeg geword het om te kan voortplant, was mense in Wes-Afrika wat sekelselsiekte het.
    Boeregroete

    Semper fidelis. Semper paratus.

    HEBREňRS 6:19 "...en ons het dit as 'n anker van die siel wat veilig en vas is en ingaan tot binnekant die voorhangsel..."

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    Verstek Ant: Drepanositose (en hoekom dit belangrik is)

    Hierdie seuntjie het baie waarskynlik aan die siekte gelei.
    Top-atleet (12) sak inmekaar, sterf op skoolveld
    2011-01-27 00:11
    Marietie Louw-Carstens


    ’n 12-jarige top-atleet van ’n laerskool in Limpopo is dood nadat hy op die atletiekveld inmekaargesak het.

    Emmanuel Maroga is eergister omstreeks 14:00 by die Steelpoort Akademie, voorheen die Laerskool Steelpoort, naby Burgersfort, dood.

    Hy het vir ’n atletiekbyeenkoms wat oormŰre in Mariepskop gehou word, geoefen.

    Die oorsaak van sy dood bly onbekend.

    Mnr. Anton Alberts, skoolhoof, het gister gesÍ Emmanuel se dood is ’n groot skok vir almal by die skool.

    “Hy was top-fiks en ons beste langafstand-atleet in die o.12-kategorie.”

    Alberts het gesÍ onderwysers wat gesien het hoe Maroga inmekaarsak, het onmiddelik mond-tot-mond-asemhaling begin toepas, maar het hy nie ’n polsslag gehad nie. NŠ ’n hele ruk se mond-tot-mond-asemhaling het hy weer ’n flou polsslag gehad, maar is toe dood, het Alberts gesÍ. Nooddienswerkers het gou by die skool opgedaag.

    Alberts het gesÍ Emmanuel het geen onderliggende siektes gehad waarvan hulle geweet het nie.

    “Hy was ’n oulike seun en ’n uiters goeie atleet.” Hy was van gr.1 ’n leerling aan die skool.

    Klasmaats van Emmanuel en onderwysers moes gister berading kry.

    Gistermiddag se atletiekoefening is afgestel ter herinnering aan Emmanuel.

    Alberts het gesÍ Emmanuel was toegewyd aan sy atletiek. Hy het ook landloop beoefen en rugby gespeel. “Hy het gesÍ hy wil vanjaar ’n goue medalje by die interlaer-byeenkoms wen. Die skool gaan ’n goue medalje en sertifikaat vir sy ma gee.”

    Me. Mathilda Maroga, Emmanuel se ma, was gistermiddag te geskok om oor haar seun se dood te praat. Sy is ’n enkelouer en woon in ’n nedersetting buite die dorp.

    Die polisie sal ’n geregtelike doodsondersoek instel om vas te stel wat Emmanuel se dood veroorsaak het.

    Teen druktyd is geen begrafnisreŽlings nog getref nie.
    http://www.beeld.com/Suid-Afrika/Nuu...lveld-20110126

  8. #8
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    Verstek Ant: Drepanositose (en hoekom dit belangrik is)

    Kwoteer Oorspronklik gepos deur Rooi Jan Bekyk pos
    Hierdie seuntjie het baie waarskynlik aan die siekte gelei.
    Tipes afrika.Hy verdien nie die medalje nie maar dit gaan tog vir hom gegee word.Wat n voorbeeld.

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    Verstek Ant: Drepanositose (en hoekom dit belangrik is)

    Is dit wat hier gebeur het? Sal ons ooit die waarheid hoor indien dit was?

    Soccer star Muamba in critical condition after collapse during FA Cup match
    March 17, 2012



    An English soccer match between top-flight teams Bolton and Tottenham was abandoned on Saturday after a player suffered a possible heart attack on the pitch before halftime.

    Bolton midfielder Fabrice Muamba was taken to hospital, the Premier League club confirmed, after medics came onto the field to try to revive him.

    It later released a statement saying Muamba was in "critical condition" in intensive care.

    "Bolton Wanderers can confirm that Fabrice Muamba has been admitted to the heart attack center at London Chest Hospital where he is currently in a critically ill condition in intensive care," the club's website reported.
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    "No further information will be issued at this stage. The club has requested the media to respect his family's privacy at this time."

    The 23-year-old from the Democratic Republic of Congo, who has represented England at under-21 level, fell to the floor in the 41st minute with no other players near him.

    Referee Howard Webb consulted both teams before calling off the match in London, which was a quarterfinal tie in England's prestigious knockout competition, the FA Cup.

    A member of CNN World Sport's London staff was at the match, and described the situation.

    "We were situated on the halfway line ... Fabrice Muamba just hit the deck out of nowhere," assistant producer Zayn Nabbi said in a phone interview.

    "We realized quite quickly that this was serious because the medical staff all rushed on and they were waved onto the field by the Tottenham players. From what we saw they were trying to resuscitate Fabrice Muamba."
    http://articles.cnn.com/2012-03-17/f..._s=PM:FOOTBALL
    Last edited by Rooi Jan; 19 Mar 2012 at 20:46.

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