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Connective Tissue Disorders

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ironjustice

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Oct 22, 2009, 9:18:36 AM10/22/09
to
This says JAK2 mutation is KNOWN / proven to cause connective tissue
disease / "prequel to the connective tissue disorders" ..
JAK2 mutation causes erythrocytosis / increased red blood cell
production ..
THUSLY .. one can **conclusively** say ..

Erythrocytosis has been NOW shown to be a possible prequel to
connective tissue disease ..

Too many red blood cells / erythrocytosis is a form of iron overload.

Will Jill come tumbling after? The case for a JAK2-type
mutation as a prequel to the connective tissue disorders.
Med Hypotheses. 2009 Nov;73(5):651-4.
Epub 2009 May 30. McQueen FM, Dalbeth N.
Dept. of Molecular Medicine and Pathology,
University of Auckland, 85 Park Rd., Grafton, Auckland, New Zealand.
f.mc...@auckland.ac.nz

The JAK2 [V617F] mutation has recently been recognised as critical
to the pathogenesis of the myeloproliferative disorders (MPDs).
Thus, a common mutation affecting a haematopoietic precursor stem
cell
is capable of giving rise to diverse clinical phenotypes.
In this hypothesis paper, we propose that a similar mutation affecting
a
stem cell precursor, most likely of the B cell lineage, could underlie
the
development of the connective tissue disorders which could be
regarded
as "lymphoproliferative" disorders.
Consistent with this hypothesis is the observation that there are
similarities
between the myeloproliferative disorders and the connective tissue
disorders
in terms of their biological behaviour.
Diseases within each family can transform into each other and
sometimes
into haematological malignancies (most often B cell origin non-
Hodgkins
lymphoma for the connective tissue disorders and acute myeloid
leukemia
for the myeloproliferative disorders).
The timecourse for development of the connective tissue disorders
involves
a long latent period when autoantibodies are present (anti-CCP and
ANA)
possibly reflecting production by a B cell clone.
A similar time-dependent increase in clonal dominance has been
described
in erythroblastic clones taken from the bone marrow of polycythemia
vera
patients, long before the onset of clinical disease.
Evidence of B cell clonality has been described in bone marrow
samples
from rheumatoid arthritis patients and from glandular biopsies from
those
with Sjogren's syndrome.
Moreover, pseudofollicles containing activated B cells are features
of
rheumatoid synovial membrane and have also recently been described in
subchondral bone where they are associated with macrophages, T cells
and osteoclasts.
The success of B cell depletion therapy in rheumatoid arthritis and
systemic
lupus erythematosus is also strong circumstantial evidence for this
hypothesis.

PMID: 19482442


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


fer...@paris.com

unread,
Oct 22, 2009, 3:11:59 PM10/22/09
to
"This says JAK2 mutation is KNOWN / proven to cause connective tissue
disease / "prequel to the connective tissue disorders" ..
JAK2 mutation causes erythrocytosis / increased red blood cell
production ..
THUSLY .. one can **conclusively** say ..

Erythrocytosis has been NOW shown to be a possible prequel to
connective tissue disease ..

Too many red blood cells / erythrocytosis is a form of iron overload."

Oh my dear, how you have indeed outdone yourself this time; thusly
indeed.

"Med Hypotheses"

Is a journal devoted to educated guesses, not wrong in itself but not
anything to get too excited about and thusly no conclusively dance is in
order.

Thusly this would be a spray gun shooting blanks, conclusively.

ironjustice

unread,
Oct 22, 2009, 3:21:22 PM10/22/09
to
Erythrocytosis has been NOW shown to be a possible prequel to
connective tissue disease ..

Too many red blood cells / erythrocytosis is a form of iron overload.

Will Jill come tumbling after? The case for a JAK2-type


mutation as a prequel to the connective tissue disorders.
Med Hypotheses. 2009 Nov;73(5):651-4.
Epub 2009 May 30. McQueen FM, Dalbeth N.
Dept. of Molecular Medicine and Pathology,
University of Auckland, 85 Park Rd., Grafton, Auckland, New Zealand.

f.mcqu...@auckland.ac.nz

Ken

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Oct 22, 2009, 5:21:14 PM10/22/09
to
Spamming Canuck Cocksucker

fer...@paris.com

unread,
Oct 22, 2009, 7:29:14 PM10/22/09
to
"This says JAK2 mutation is KNOWN / proven to cause connective tissue
disease / "prequel to the connective tissue disorders" ..
JAK2 mutation causes erythrocytosis / increased red blood cell
production ..
THUSLY .. one can **conclusively** say ..

Erythrocytosis has been NOW shown to be a possible prequel to
connective tissue disease ..

Too many red blood cells / erythrocytosis is a form of iron overload."

Oh my dear, how you have indeed outdone yourself this time; thusly

ironjustice

unread,
Oct 24, 2009, 11:24:26 AM10/24/09
to
Atheist shteating .. dweeeeeeb ..

Giiiiiiit ..

This says JAK2 mutation is KNOWN / proven to cause connective tissue
disease / "prequel to the connective tissue disorders" ..
JAK2 mutation causes erythrocytosis / increased red blood cell
production ..

THUSLY .. one can **conclusively** say ..

Erythrocytosis has been NOW shown to be a possible prequel to
connective tissue disease ..

Too many red blood cells / erythrocytosis is a form of iron overload.

Will Jill come tumbling after? The case for a JAK2-type

Ken

unread,
Oct 24, 2009, 11:38:02 AM10/24/09
to
Spamming Mentally Defective Spamming Canuck Dickhead

ironjustice

unread,
Oct 25, 2009, 4:09:48 PM10/25/09
to
On Oct 24, 8:24 am, ironjustice <teamtan...@hotmail.com> wrote:
pseudofollicles containing activated B cells are features of
rheumatoid synovial membrane <<

One might NOW then theorize / reverse engineer THAT .. ? .. IF the RF
factor TOO is raised THEN it would also give credence to this RF
factor to be a merker for MORE than simple arthritiis and may be a
marker for .. increased red blood cell production / altitude
syndrome .. in SOME people ..

http://groups.google.com/group/sci.med.laboratory/browse_thread/thread/2e44e3d4fb94482d

Anyone have any ideas as to .. why .. the RF .. factor .. the
'marker'
FOR .. "rheumatoid arthritis" ... would seemingly be affected BY ..
altitude .. ?

http://www.labtestsonline.org/understanding/analytes/rheumatoid/test....


WHY would the people in the higher than sea level .. just
'coincidentally' be .. having .. the increased rate of what is
thought
to be THE marker of a .. genetic predisposition .. ? .. TO ..
rheumatoid arthritis .. AS .. they .. rise .. higher and higher .. ?


Or .. does .. altitude ITSELF .. raise RF .. factor .. ?


<<snip>>
observed that the prevalence of rheumatoid nodules, RF, and erosive
arthritis in Africa increased along an altitude gradient from sea
level (Nigeria) to high-altitude regions (Uganda and Lesotho). They
postulated that it was the absence of tropical infections at high
altitudes that predisposed to more severe disease.
<<snip>>


http://www.medscape.com/viewarticle/448141_4


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

> Atheist shteating .. dweeeeeeb ..
>
> Giiiiiiit ..
>
> This says JAK2 mutation is KNOWN / proven to causeconnectivetissuedisease/ "prequel to theconnectivetissuedisorders" ..


> JAK2 mutation causes erythrocytosis / increased red blood cell
> production ..
>
> THUSLY .. one can **conclusively** say ..
>
> Erythrocytosis has been NOW shown to be a possible prequel toconnectivetissuedisease..
>
> Too many red blood cells / erythrocytosis is a form of iron overload.
>
> Will Jill come tumbling after? The case for a JAK2-type
> mutation as a prequel to theconnectivetissuedisorders.
> Med Hypotheses. 2009 Nov;73(5):651-4.
> Epub 2009 May 30. McQueen FM, Dalbeth N.
> Dept. of Molecular Medicine and Pathology,
> University of Auckland, 85 Park Rd., Grafton, Auckland, New Zealand.
> f.mcqu...@auckland.ac.nz
>
> The JAK2 [V617F] mutation has recently been recognised as critical
> to the pathogenesis of the myeloproliferative disorders (MPDs).
> Thus, a common mutation affecting a haematopoietic precursor stem
> cell
> is capable of giving rise to diverse clinical phenotypes.
> In this hypothesis paper, we propose that a similar mutation
> affecting
> a
> stem cell precursor, most likely of the B cell lineage, could
> underlie
> the

> development of theconnectivetissuedisorders which could be


> regarded
> as "lymphoproliferative" disorders.
> Consistent with this hypothesis is the observation that there are
> similarities
> between the myeloproliferative disorders and theconnectivetissue
> disorders
> in terms of their biological behaviour.
> Diseases within each family can transform into each other and
> sometimes
> into haematological malignancies (most often B cell origin non-
> Hodgkins

> lymphoma for theconnectivetissuedisorders and acute myeloid

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