Spleen cell proliferation assays

K. Weber kweber at efn.org
Tue Mar 17 15:01:00 EST 1998

On 12 Mar 1998, J.S Good wrote:

> Do you have any experience with or knowledge of assays of proliferation
> which are based on incorporation of BrdU detected by ELISA as opposed to
> assays based of tritiated thymidine? For example, the kit available from
> Boehringer Mannheim.
> Any info welcome!
I am a lay-person involved in the patient community for Myalgic
Encephelopathy.  We have had deaths from  ruptured spleens, and a large
number of people with very enlarged spleens.  I understand that these
problems are rare in the general population, but wonder how spleen-cell
proliferation is generated.  0If you are not familiar enough with M.E.
perhaps you could talk about how this occurs in sicklemia or sickle-cell
anemia.  M.E. is so complex that sometimes we need to ask questions that
are shots in the dark.  We think that people of color tend to be more ill
than white people.  In a preliminary CDC study, they were twice as sick as
white people.  It is my personal belief that hypoxia, available from a
wide range of etiologies is what may trigger or be n important trigger of
M.E.  The simple hypoxia available for infections from poor lung
function, etc. can be complicated by malformed hemoglobin cells.  There
are a number of types of malformation in M.E.  Some of these are caused by
abnormalities of nitrogen in the blood-- either high or low in M.E.  It
would seem to be me possible for there to be some link here.  Sever anemia
with cupaform hemoglobin cells and abnormalities in red and white cell
ratios are no more than rare in CFS.  At the time that I had a very
massive thrombosis in my legs, I had three times the number of red cells
as white cells, while actually anemic.  I know of other cases of this
type, and of clusters of this type of blood deformity in the young and
middle aged.  

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