Talk:Sickle cell disease: Difference between revisions

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Date	Process	Result
February 12, 2005	Peer review	Reviewed

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Just as a comment for further discussion, I did hemoglobin research for about 4 and a half years. I recall a conversation (ca 1993 or 1994) with Professor Gary Ackers (at the time, chair of biochemistry and molecular biophysics at Washington University in St Louis Medical School, and one of the leading experts on hemoglobin cooperativity) about a paper, in which they mapped the site of action of the digestive enzyme the malaria parasite used on hemoglobins (as Hb is what they eat). It turns out that in the process of polymerization (HB S now, the sickle cell Hb), the polymerization caps the site of digestion, making Hb a poor meal for the parasite. That, to my understanding, was the way that in heterozygous individuals the mutation had selective pressure against the parasite. It slowed the rate of growth, because they couldn't feed as effectively on heterozygous individuals. Inter-cell death seems to be a poor mechanism for selective pressure, as few cells are sickled in heterozygous individuals. dwmyers live your life to the fungas max.

Simple test for sickle cell carriers

I read this in a test on genetics in GCSE Biology. If a sample of a carrier's blood is kept in low oxygen conditions, a few cells with become sickle shaped. This is roughly what the test said:

A couple are worried that they might pass on sickle cell anaemia to their children, so they had blood samples taken for a test. The father's sample developed sickle cells in low oxygen conditions whereas the mother's didn't. What does this mean?

Of course, it meant that the couple's children would a half chance of becoming a carrier, but won't develop the disease. But since I can't obtain the paper, I can't prove that it was there, but I doubt that it's a lie.

Cerebral vasculopathy

doi:10.1111/bjh.12300 Br J Haem 14:54, 25 April 2013 (UTC)

More treatment, vicar?

doi:10.1111/bjh.12413 JFW | T@lk 19:28, 17 June 2013 (UTC)[reply]

Vaso-occlusion

doi:10.1182/blood-2013-05-498311 - review in Blood. JFW | T@lk 16:08, 8 December 2013 (UTC)[reply]

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 == older entries ==
-Just as a comment for further discussion, I did hemoglobin research for about 4 and a half years. I recall a conversation (ca 1993 or 1994) with Professor Gary Ackers (at the time, chair of biochemistry and molecular biophysics at Washington University in St Louis Medical School, and one of the leading experts on hemoglobin cooperativity) about a paper, in which they mapped the site of action of the digestive enzyme the malaria parasite used on hemoglobins (as Hb is what they eat). It turns out that in the process of polymerization (HB S now, the sickle cell Hb), the polymerization caps the site of digestion, making Hb a poor meal for the parasite. That, to my understanding, was the way that in heterozygous individuals the mutation had selective pressure against the parasite. It slowed the rate of growth, because they couldn't feed as effectively on heterozygous individuals. Inter-cell death seems to be a poor mechanism for selective pressure, as few cells are sickled in heterozygous individuals. [[User:dwmyers|dwmyers]]
+Just as a comment for further discussion, I did hemoglobin research for about 4 and a half years. I recall a conversation (ca 1993 or 1994) with Professor Gary Ackers (at the time, chair of biochemistry and molecular biophysics at Washington University in St Louis Medical School, and one of the leading experts on hemoglobin cooperativity) about a paper, in which they mapped the site of action of the digestive enzyme the malaria parasite used on hemoglobins (as Hb is what they eat). It turns out that in the process of polymerization (HB S now, the sickle cell Hb), the polymerization caps the site of digestion, making Hb a poor meal for the parasite. That, to my understanding, was the way that in heterozygous individuals the mutation had selective pressure against the parasite. It slowed the rate of growth, because they couldn't feed as effectively on heterozygous individuals. Inter-cell death seems to be a poor mechanism for selective pressure, as few cells are sickled in heterozygous individuals. [[User:dwmyers|dwmyers]] live your life to the fungas max.
 == Simple test for sickle cell carriers ==