Just For Fun--Blood Bank Quiz Game!

[LisaM]

I'm afraid not Lisa; the antigen/antibody reactions of all of these Blood Group Systems are enhanced by the action of enzymes. Those that are sensitive are Chido/Rodgers (although some very rare, really strong examples of anti-Ch will react with papain-treated red cells), the Indian BGS, JMH and Xg. The low incidence antigen in the 701 series, Bp(a), is also senstivie to these enzymes.

:redface::redface:

Yeah, I figured I was grasping at straws--haven't done anything with enzymes, really, in my blood bank experience.

[Eagle Eye]

I'm afraid not Lisa; the antigen/antibody reactions of all of these Blood Group Systems are enhanced by the action of enzymes. Those that are sensitive are Chido/Rodgers (although some very rare, really strong examples of anti-Ch will react with papain-treated red cells), the Indian BGS, JMH and Xg. The low incidence antigen in the 701 series, Bp(a), is also senstivie to these enzymes.

:redface::redface:

the answer I was looking for is : Chido/Rodgers, JMH, and Xga.....So you ROCK Malcolm!!!!

[Deny Morlino]

Thanks for the attempt Lisa as I was struggling with that one as well. Can definitely tell there are people here that work in reference labs and have much more experience with these things I appreciate each new thing I learn from you folks, so thanks.

[LisaM]

Thanks for the attempt Lisa as I was struggling with that one as well. Can definitely tell there are people here that work in reference labs and have much more experience with these things I appreciate each new thing I learn from you folks, so thanks.

I think I actually misinterpreted the question--LOL! I went back and read it again and I must've taken the enzyme reference of "sensitive to" as being "enhanced by" instead of "neutralized" as intended. --Not that I would've had an easier time finding the answer, mind you, but oh well! (And also proof that I should not be taking quizzes and doing continuing education between the hours of 10pm and midnight--the brain starts to drift a little at that time frame!!!)

[Malcolm Needs ☆]

I think I actually misinterpreted the question--LOL! I went back and read it again and I must've taken the enzyme reference of "sensitive to" as being "enhanced by" instead of "neutralized" as intended. --Not that I would've had an easier time finding the answer, mind you, but oh well! (And also proof that I should not be taking quizzes and doing continuing education between the hours of 10pm and midnight--the brain starts to drift a little at that time frame!!!)

Love the new avatar Lisa.

:):)

[Malcolm Needs ☆]

QUESTION: What is the cause of lea+b+?

There are four types of Le(a+b+).

One is that seen in babies/neonates. Almost all babies are Le(a-b-), but those that are destined to become Le(a-b+) in later life tend to go through stages that are Le(a+b-), Le(a+b+) and then Le(a-b+), as the alpha(1,3/1,4)fucosyltransferase enzymes start to mature and transfer the immunodominant sugar residues.

The second is sometimes seen in pregnancy (or, rather, just after pregnancy) when the high level of plasma lipoproteins seen during pregnancy begins to diminish, and an Le(a-b+) lady goes from being Le(a-b-) back to Le(a-b+), rather in the same fashion as above.

The third is sometimes seen after either a transfusion or a bone marrow transplant, when Le(a+b-) transfused blood, or transplanted red cells, take up the Le(a-b+) phenotype from the recipient (the Lewis type of the recipient does not change).

The fourth is often seen in the Far East, where about 16.8% of the population are Le(a+b+) (with a slightly weakened Le( antigen), and this is due to a mutation in the FUT2 (SE) gene: 385A>T, resulting in Ile129Phe.

What is unusual about the Duffy genotype of individuals who are Fy(a-b-) from Papua New Guinea?

:confused::confused::confused:

[Dr. Pepper]

The mutation evolved independently of and is different from other Duffy null mutations. A mutation of the FYA gene instead of the FYB gene? I'm on thin ice here.

[LaraT23]

Hmm, I agree, found that the only Fya-Fyb- resulting from a GATA mutationon the FYA gene was found in Papua New guinea.

I supposed I should post a question:

What blood group antigens are carried on membrane protein CHIP 28, which also carries Aquaporin-1?

[Malcolm Needs ☆]

Phil and Lara, you are both absolutely correct (thought that one would take much longer to crack, so very well done to both of you)!!!!!!!!!!!!!!!!!!!!!!!!!!

:D:D:D:D:D

[Malcolm Needs ☆]

Hmm, I agree, found that the only Fya-Fyb- resulting from a GATA mutationon the FYA gene was found in Papua New guinea.

I supposed I should post a question:

What blood group antigens are carried on membrane protein CHIP 28, which also carries Aquaporin-1?

I know this one, but I'm going to leave it for a while so that others get a chance to answer it. Just to say that it is another Blood Group System that was given the wrong name because of poor handwriting on the sample tube (like Lutheran, which should be Lutteran)!

:cool::cool::cool::cool:

[LisaM]

Love the new avatar Lisa.

:):)

Heh! I pulled off the wig for good, since my hair has grown back. It's not quite long enough for my liking and I do look a bit like my Grandmother, but it seems to be growing fast!

[L106]

Looking good, Lisa!!!!!!

Donna

[Han Chau]

Hmm, I agree, found that the only Fya-Fyb- resulting from a GATA mutationon the FYA gene was found in Papua New guinea.

I supposed I should post a question:

What blood group antigens are carried on membrane protein CHIP 28, which also carries Aquaporin-1?

Is it Colton blood group antigens?

[Han Chau]

There are four types of Le(a+b+).

One is that seen in babies/neonates. Almost all babies are Le(a-b-), but those that are destined to become Le(a-b+) in later life tend to go through stages that are Le(a+b-), Le(a+b+) and then Le(a-b+), as the alpha(1,3/1,4)fucosyltransferase enzymes start to mature and transfer the immunodominant sugar residues.

The second is sometimes seen in pregnancy (or, rather, just after pregnancy) when the high level of plasma lipoproteins seen during pregnancy begins to diminish, and an Le(a-b+) lady goes from being Le(a-b-) back to Le(a-b+), rather in the same fashion as above.

The third is sometimes seen after either a transfusion or a bone marrow transplant, when Le(a+b-) transfused blood, or transplanted red cells, take up the Le(a-b+) phenotype from the recipient (the Lewis type of the recipient does not change).

The fourth is often seen in the Far East, where about 16.8% of the population are Le(a+b+) (with a slightly weakened Le( antigen), and this is due to a mutation in the FUT2 (SE) gene: 385A>T, resulting in Ile129Phe.

What is unusual about the Duffy genotype of individuals who are Fy(a-b-) from Papua New Guinea?

:confused::confused::confused:

Malcolm, in Aboriginal Australian, when both Lewis and Secreted genes are present, some part of the Le-a still remains instead of transforming all to Le-b, and that's why they are Le (a+b+). Does it belong to the 4th condition that you mentioned or another situation?

[Malcolm Needs ☆]

Malcolm, in Aboriginal Australian, when both Lewis and Secreted genes are present, some part of the Le-a still remains instead of transforming all to Le-b, and that's why they are Le (a+b+). Does it belong to the 4th condition that you mentioned or another situation?

Yes!

:D:D:D:D

[Dr. Pepper]

Malcolm, I had heard the story of the Lutheran misnaming but not Colton. What should Colton have been?

[Malcolm Needs ☆]

Malcolm, I had heard the story of the Lutheran misnaming but not Colton. What should Colton have been?

Apparently, it should have been CAlton.

:eek:

[Malcolm Needs ☆]

Is it Colton blood group antigens?

We need another question now.

[LaraT23]

What blood group antigens are missing from the erythrocytes of patients with PNH? Why?

[KLCarter]

OK, the Leach phenotype is GPC/D deficiency (and yes, I had to look it up).

I'll go for something a smidge easier. What is the genetic relationship between Fy and Rh?

Both Fy and Rh are on chromosome 1. anti-Fy5 does not react with Rh null cells regardless of the Fy type of the Rh null cells

Now how about something from the Lutheran system - Of the 3 mechanisms for Lu(a-b-) phenotype, which is the one that can develop an anti-Lu3?

[Malcolm Needs ☆]

Both Fy and Rh are on chromosome 1. anti-Fy5 does not react with Rh null cells regardless of the Fy type of the Rh null cells

Now how about something from the Lutheran system - Of the 3 mechanisms for Lu(a-b-) phenotype, which is the one that can develop an anti-Lu3?

I'll answer this one, rather than Lara's, on the grounds that firstly (I think) Lara's question is the more difficult, and secondly, I was talking about just this at a meeting last Thursday, and so those that are UK members from the Tooting Reference Centre area and were at the meeting (at least three, and possibly more) should know the answer.

There are three kinds of Lu(a-b-), only one of which is a true Lu(a-b-); the others one can adsorb and elute Lutheran antibodies from the red cells.

The most common, and the first described, is the so-called "dominant" form of Lu(a-b-), caused by the inheritance in either the homozygous or heterozygous state of the In(Lu) gene (a gene that also causes weakening of other blood group antigens, viz P1, AnWj, Indian, Knops, Cs(a) and MER2). This is almost unique in as much as the propositus also happened to be the main author of the paper (Crawford MN, Greenwalt TJ, Sasaki T, Tippett P, Sanger R, Race RR. The phenotype Lu(a-b-) together with unconventional Kidd groups in one family. Transfusion, Philad. 1961; 1: 228-232). Such individuals cannot produce anti-Lu3.

Now, come on the members from the Tooting area; answer Lara's question.

The second type described is the "genuine" recessive type of Lu(a-b-). These individuals inherit a silent LU gene in the homozygous state (rather than LUA and/or LUB). Such individuals have red cells that do not adsorb Lutheran antibodies. This type was first descibed by Darnborough et al in 1963 (Darnborough J, Firth R, Giles CM, Goldsmith KLG, Crawford MN. A 'new' antibody anti-LuaLub and two further examples of the genotype Lu(a-b-). Nature 1963; 198: 796). As could be deduced from the title of this paper, such individuals can (and do) make anti-Lu3.

The third type is the X-linked Lu(a-b-), which has only ever been described in one family (Norman PC, Tippett P, Beal RW. An Lu(a-b-) phenotype caused by an X-linked recessive gene. Vox Sang 1986; 51: 49-52). Such individuals cannot make anti-Lu3.

I attach a cartoon of the X chromosome to show where this gene is situated.

:D:D:D:D

XKCH.ppt

[LisaM]

Ok, I'll post the next question: How many antigens are in the Diego system and what year was the first one discovered?

[LaraT23]

There are seven antigens in the Diego system - Dia, Dib, Wra, Wrb, Wda, Rba, WARR. I am finding the first one discovered in 1991 but not sure if that is correct. Help me out anyone?

[adiescast]

What blood group antigens are missing from the erythrocytes of patients with PNH? Why?

OK, I'll take a stab at this one. The why has to be because of the absence of the glycosylphosphtidylinositol that would form the anchor for the rest of the antigen. The antigens affected are Cromer, YT, Holley-Gregory, JMH, and Dombrock.

Wow, that one was hard!

In the same vein, what other hematologic disease are PNH patients more susceptible for?

[LisaM]

There are seven antigens in the Diego system - Dia, Dib, Wra, Wrb, Wda, Rba, WARR. I am finding the first one discovered in 1991 but not sure if that is correct. Help me out anyone?

If this is accurate, there's 21 and the year is 1955--that's where I got the info:

http://en.wikipedia.org/wiki/Diego_antigen_system