Systemic Lupus Erythematosus and Tissue Catabolism

[Adminஐﻬ]

On Tue, Mar 18, 2008 at 8:48 AM, tyler malcolm <XXXXXX@ptd.net> wrote:

 

Systemic Lupus Erythematosus and Tissue Catabolism

Copyright 1985 by William Tyler Malcolm

 
A 90% female incidence and a diversity of autoantigens are unusual features of the autoimmune disorder systemic lupus erythematosus (SLE).  The link between estrogenic metabolites and immune stimulation is far too weak to account for SLE's overwhelming female prevalence (besides, any such causal relationship would make all other autoimmune disorders 90% female as well).  The consistent occurrence of the same set of autoantigens and the existence of animal models for SLE suggest that it may be related to a fundamental process.  The immunological aspect of tissue catabolism during necrotic clean up and necrobiotic removal may be this process since most of the autoantigens of SLE are intracellular substances and because female histology is characterized by a high amount of menstrual and pregnancy-related cell turnover in many tissues (endometrium, myometrium, cervical mucus glands, vagina, ovary, mammary epithelia).  Since these processes are driven by sex steroids the studies linking linking these hormones and oral contraceptives to SLE's predisposition or progression make sense when viewed through the steroids' stimulatory or antagonistic effects on the normal hyperplastic processes, rather than through their direct influences on the immune system.  Since tissue catabolism is such a fundamental and certain process it is unlikely that a diverse immune response is generated de novo each time a cell turns over; rather, this complicated response is probably a set of concerted actions narrowly controlled, steadily maintained, and suitably modulated.  The circulating anticoagulants often increased in SLE and the other targets of autoantibody such as platelets, erythrocytes, and lymphocytes fit this hypothesis since one would expect that they function in tissue catabolism, or are normally present at the locus, or are themselves the objects of overly aggressive immune-related turnover mechanisms.  Predictably, complement would function in cell turnover and SLE, unlike most other autoimmune disorders, shows abnormalities in serum complement levels and C3b receptors.  Exposure of the T antigenic determinant (MN blood group precursor) is a possible mechanism of cell turnover.  Humans maintain anti-T IgM even in the absence of disease and females have higher IgM levels than males.  Normally, the T antigen is masked and the pentameric anti-T IgM is inaccessible to tissue cells.  The acidic (trauma environment) or enzymatic unmasking of T followed by its complexing with anti-T IgM at a locus of microtrauma or a site of increased vascular permeability should trigger complement fixation.  It is difficult to imagine why the T antigenic determininant exists and the anti-T IgM is maintained if the resulting complex does not serve some purposeful function, such as initiating cell turnover.  A possible explanation of the reciprocal incidences of breast cancer and SLE between black and white women is that a more active and efficient cell turnover process may reduce the risk of a fully progressed malignancy but increase the chance of SLE.  This cell turnover concept is also useful in understanding the gender differences in the incidences of many other malignancies.
Thank you Mr. Malcom for your contribution, it is deeply appreciated for all to read.
~Kathy

[Adminஐﻬ]

Hello Malcom,
Our ex President Bush Sr. and his wife Barbara Bush had a dog named Milly which had the canine lupus. Just curious your thoughts on this if the Tissue Catabolism would apply to the canines as well.

  Looking forward to your reply to the board

[Tyler]

Cell turnover is a fundamental process common to all animals.  Instict tells me that an overactive deregulation of the immune system's role in this process would result in lupus-like symptoms in any species.  Canine lupus does resemble human SLE in that it affects multiple organ systems, has a vast range of symptoms and severities, and is difficult to diagnose (the vets also call it The Great Imitator).  I'm giving you a quick answer, but I would like to research this further to see if there is a gender difference in dogs and, if so, try to better understand the disease in the context of canine reproductive biology.  Messy stuff:  Male or female?  Spayed?  Neutered?  Age of onset?  Is it breed-specific? 

[Adminஐﻬ]

Cell turnover is a fundamental process common to all animals.  Instict tells me that an overactive deregulation of the immune system's role in this process would result in lupus-like symptoms in any species.  Canine lupus does resemble human SLE in that it affects multiple organ systems, has a vast range of symptoms and severities, and is difficult to diagnose (the vets also call it The Great Imitator).  I'm giving you a quick answer, but I would like to research this further to see if there is a gender difference in dogs and, if so, try to better understand the disease in the context of canine reproductive biology.  Messy stuff:  Male or female?  Spayed?  Neutered?  Age of onset?  Is it breed-specific? 

Ty,
I saw you online as I was leaving to go to my Vet.
I have to see him again next week, I'll ask him if has treated any dogs for lupus and if so can he give me any info regarding those dogs.

It would be one vet's opinion anyway to start with.
THANK YOU for posting

[SunniPearl2]

My Sister's dog passed away from Lupus, she had skin Lupus, to sad, my uncle insists we both have Lupus from her dog    But since the Dioctors said my sister does not have Lupus they said it's fibro? what ever.....

[Adminஐﻬ]

SLE/Tissue Catabolism and Complementary Biomolecules as Potential Autoantigens were sent to a number of NIH institutes and offices decades ago and IN THEORY should be public documents under the Freedom of Information Act...

http://cocatalog.loc.gov/cgi-bin/Pwebrecon.cgi?DB=local&PAGE=First
Highlight SEARCH BY NAME and type "Malcolm William" or do a TITLE SEARCH "SLE and Tissue Catabolism"
Thank you Tyler for the link, but most of all your knowledge & submissions on behalf of us patients that one day this is the true reason behind Lupus existance and that a cure will be found  KUDOS Tyler!

[Debby]

SLE/Tissue Catabolism and Complementary Biomolecules as Potential Autoantigens were sent to a number of NIH institutes and offices decades ago and IN THEORY should be public documents under the Freedom of Information Act...

http://cocatalog.loc.gov/cgi-bin/Pwebrecon.cgi?DB=local&PAGE=First
Highlight SEARCH BY NAME and type "Malcolm William" or do a TITLE SEARCH "SLE and Tissue Catabolism"
Thank you Tyler for the link, but most of all your knowledge & submissions on behalf of us patients that one day this is the true reason behind Lupus existance and that a cure will be found  KUDOS Tyler!

#   Name Heading    Author    Full Title    Date
[ 1 ]    Malcolm, William Tyler, 1958-    

 

   Adolescent bone neoplasms and skeletal growth.    1985
[ 2 ]    Malcolm, William Tyler, 1958-    

 

   Breast carcinomas as uncontrolled menstrual proliferations.    1984
[ 3 ]    Malcolm, William Tyler, 1958-    

 

   CF, C1[superscript]-, and ACE.    1985
[ 4 ]    Malcolm, William Tyler, 1958-    

 

   Complementary biomolecules as potential autoantigens / by William Tyler Malcolm.    1985
[ 5 ]    Malcolm, William Tyler, 1958-    

 

   Neoplasms as uncontrolled regenerative hyperplasia / William Tyler Malcolm.    1984
[ 6 ]    Malcolm, William Tyler, 1958-    

 

   Systemic lupus erythematosus and tissue catabolism / by William Tyler Malcolm.    1985

             there is no way I can access these to read 

[Adminஐﻬ]

Deb,
We can only look up and verify the Author or the article.
The past decades of articles submitted should be made public under the Freedom of Information Act.

Other than not being able to read his work except the SLE/Tissue Catabolism posted below, it is pretty impressive, eh?
I wish the future was NOW so we could see for ourselves if his theory is correct.
Then a cure could be found to help millions
Time will tell. He wrote that back in the early 1980's when he was in his twenties. (Even more impressive if I say so myself!)   

[Adminஐﻬ]

Here is a link for everyone to check out, notice the dates these researchers are studying the same theory Tyler thought of and had copyrighted back in the 1980's.
http://www.springerlink.com/content/u5epbu5e0kx2u6b6/
Here is info on Tyler when he filed:


> Type of Work:      Text
>
> Registration Number / Date:
>                   TXu000218385 / 1985-12-02
>
> Title:             Complementary biomolecules as potential autoantigens /
> by
>                      William Tyler Malcolm.
>
> Description:       2 p.
>
> Copyright Claimant:
>                   William Tyler Malcolm
>
> Date of Creation:  1985
>
> Names:             Malcolm, William Tyler, 1958-
>
> =============================
>
>
>
> +++++++++++++++++++++++++++++
> The Library of Congress
> United States Copyright Office
> 101 Independence Ave., S.E.
> Washington, D.C. 20559-6000
> 202-707-3000

[Crockett2007]

are these researchers trying to copy Tyler's work?  I don't understand, if he had his work copyright protected back in the 80s he should get credit if there is a discovery, am I correct on the understanding here?

[Adminஐﻬ]

are these researchers trying to copy Tyler's work?  I don't understand, if he had his work copyright protected back in the 80s he should get credit if there is a discovery, am I correct on the understanding here?

Edited by Admin. It should read as :
The link below on Tyler's theory is co-discovery 
http://www.springerlink.com/content/u5epbu5e0kx2u6b6/
Tyler is a VERY smart and intellagent man...... and did I mention he has a great sense of humor too? 

[Debby]

thank you for such detailed information! wow Tyler was copy writing his study
systemic lupus erythematosus and tissue catabolism 20 +years before these other two researchers. I can't wait to see how this plays out.
If I were Tyler I would write to them and enclose his theory to show proof he wrote his first.
Keep us posted this is something I am jazzed about in hopes we have an answer, this would be something the lupus research people might be interested in talking to you.:

[Adminஐﻬ]

This article plainly states that this Stanford team is closing in on the first new lupus treatment in nearly half a century.  Does it not?  I'm not making it up.  What is that treatment?  So I read:  First it says that the goal is to identify pre-lupus people who aren't patients yet and "cure them up front" - whatever that means.  Is that it?  Is that the new treatment?  Curing people of lupus who don't have lupus?  Sounds easy.  Then it mentions something a little more specific, Rituxan, and informs us of encouraging results, but an inconclusive trial study.  Is that it?  Is that the new treatment?  Rituxan? Is it still viable?  Are there going to be more trials?  It doesn't say.  Next we move to "genetic markers" and finally to "other studies," but I still don't know what the first new lupus treatment in nearly half a century that is being closed in on by this Stanford team is  Understand:  Nothing would make me happier than news of a new and effective lupus treatment.  I just think that the introduction to this story is misleading.
http://abclocal.go.com/kgo/story?section=news/drive_to_discover&id=6271902

[Adminஐﻬ]

My Sister's dog passed away from Lupus, she had skin Lupus, to sad, my uncle insists we both have Lupus from her dog    But since the Dioctors said my sister does not have Lupus they said it's fibro? what ever.....

Found a dog site where they talkk about their dogs living with SLE
http://www.lab-retriever.net/board/sle-systemic-lupus-t7295326.html?p=1963632469#post1963632469

[Adminஐﻬ]

Last night Kimmy (3 Sisters) and I had a three way conversation with the famous Mr William Tyler Malcolm.
I must say I could listen to him talk for hours on end speaking.
Sadly there is a 3 hour gap in time zones, perhaps there will be more conversations in the future.

Thank you for the good company Kimmy & Tyler, I hope we will do it again!

And hey Ty, listening to you speak last night is like me watching a You Tube video on Richard Feynman 
http://youtube.com/watch?v=_EZcpTTjjXY&feature=related

[3sisters]

Mr. Malcolm, it it was a pleasure to talk with you on the phone. The way that you articulate things for lay people is wonderful. I also enjoyed discussing all of the cutting edge research discrepancies. 

And yes, Kathy, I too, would like to thank you and Mr. Malcolm for the good company and I certainly look forward to doing it again.

Cheers,
Kimmy

[Tyler]

Hello people, here is a fun and interesting experiment that everyone can try:  Please go Google and do an EXACT SEARCH for "systemic lupus erythematosus."  Next, do a SEARCH WITHIN for "apoptosis."  Apoptosis is the fancy technical word for cell turnover.  (Actually, the meaning isn't exact.  Apoptosis refers to the natural process of cell death, rather than ones that die from injury.  But close enough.  A dead cell is a dead cell.)

[Adminஐﻬ]

Hello people, here is a fun and interesting experiment that everyone can try:  Please go Google and do an EXACT SEARCH for "systemic lupus erythematosus."  Next, do a SEARCH WITHIN for "apoptosis."  Apoptosis is the fancy technical word for cell turnover.  (Actually, the meaning isn't exact.  Apoptosis refers to the natural process of cell death, rather than ones that die from injury.  But close enough.  A dead cell is a dead cell.)

Ah Ha!!!
This is your theory basically that you wrote about 23+ years ago, correct?

Here ya go people, just a few of many out there that are researching this

http://www3.interscience.wiley.com/journal/87510598/abstract?CRETRY=1&SRETRY=0

http://www3.interscience.wiley.com/journal/87510598/abstract?CRETRY=1&SRETRY=0

http://www3.interscience.wiley.com/journal/87510598/abstract?CRETRY=1&SRETRY=0

http://rheumatology.oxfordjournals.org/cgi/content/short/38/12/1177

http://ard.bmj.com/cgi/content/abstract/58/5/309

http://www.ncbi.nlm.nih.gov/pubmed/15308111
Here is Tyler's work registered:



> Type of Work:      Text
>
> Registration Number / Date:
>                   TXu000218385 / 1985-12-02
>
> Title:             Complementary biomolecules as potential autoantigens /
> by
>                      William Tyler Malcolm.
>
> Description:       2 p.
>
> Copyright Claimant:
>                   William Tyler Malcolm
>
> Date of Creation:  1985
>
> Names:             Malcolm, William Tyler, 1958-
>
> =============================
>
>
>
> +++++++++++++++++++++++++++++
> The Library of Congress
> United States Copyright Office
> 101 Independence Ave., S.E.
> Washington, D.C. 20559-6000
> 202-707-3000

[Tyler]

The story so far:  There is increasing evidence that links lupus to cell turnover, yet the researchers still don't know why the disease is 90% female.  I am in true disbelief, but, it is like the old saying:  "You can lead a horse to water, but you can't make it understand basic biology."

[Adminஐﻬ]

The story so far:  There is increasing evidence that links lupus to cell turnover, yet the researchers still don't know why the disease is 90% female.  I am in true disbelief, but, it is like the old saying:  "You can lead a horse to water, but you can't make it understand basic biology."

Well in high school I cut Biology class so I'm not with it on the information that is in your head. I just believe in you, reading your paper work makes sense.
I am one that is a good judgement of charactor, if it walks like a duck, talks like a duck, it must be a duck.
Now your information, talking to you and emailing you , I don't get the duck feeling.Not to mention having your Library of Congress papers to back up your claim helped me determine why I believe in you and your theory.

[Adminஐﻬ]

Bumping up Tyler's article that was copyrighted back in the 1980's when he was just in his twenties.
I've very proud of Tyler's acomplishments and I want his work to get the recognition it deserves in the Internet world. So you may see this often.
Good going Ty!
Kathy
 

On Tue, Mar 18, 2008 at 8:48 AM, tyler malcolm <XXXXXX@ptd.net> wrote:

 

Systemic Lupus Erythematosus and Tissue Catabolism

Copyright 1985 by William Tyler Malcolm

 
A 90% female incidence and a diversity of autoantigens are unusual features of the autoimmune disorder systemic lupus erythematosus (SLE).  The link between estrogenic metabolites and immune stimulation is far too weak to account for SLE's overwhelming female prevalence (besides, any such causal relationship would make all other autoimmune disorders 90% female as well).  The consistent occurrence of the same set of autoantigens and the existence of animal models for SLE suggest that it may be related to a fundamental process.  The immunological aspect of tissue catabolism during necrotic clean up and necrobiotic removal may be this process since most of the autoantigens of SLE are intracellular substances and because female histology is characterized by a high amount of menstrual and pregnancy-related cell turnover in many tissues (endometrium, myometrium, cervical mucus glands, vagina, ovary, mammary epithelia).  Since these processes are driven by sex steroids the studies linking linking these hormones and oral contraceptives to SLE's predisposition or progression make sense when viewed through the steroids' stimulatory or antagonistic effects on the normal hyperplastic processes, rather than through their direct influences on the immune system.  Since tissue catabolism is such a fundamental and certain process it is unlikely that a diverse immune response is generated de novo each time a cell turns over; rather, this complicated response is probably a set of concerted actions narrowly controlled, steadily maintained, and suitably modulated.  The circulating anticoagulants often increased in SLE and the other targets of autoantibody such as platelets, erythrocytes, and lymphocytes fit this hypothesis since one would expect that they function in tissue catabolism, or are normally present at the locus, or are themselves the objects of overly aggressive immune-related turnover mechanisms.  Predictably, complement would function in cell turnover and SLE, unlike most other autoimmune disorders, shows abnormalities in serum complement levels and C3b receptors.  Exposure of the T antigenic determinant (MN blood group precursor) is a possible mechanism of cell turnover.  Humans maintain anti-T IgM even in the absence of disease and females have higher IgM levels than males.  Normally, the T antigen is masked and the pentameric anti-T IgM is inaccessible to tissue cells.  The acidic (trauma environment) or enzymatic unmasking of T followed by its complexing with anti-T IgM at a locus of microtrauma or a site of increased vascular permeability should trigger complement fixation.  It is difficult to imagine why the T antigenic determininant exists and the anti-T IgM is maintained if the resulting complex does not serve some purposeful function, such as initiating cell turnover.  A possible explanation of the reciprocal incidences of breast cancer and SLE between black and white women is that a more active and efficient cell turnover process may reduce the risk of a fully progressed malignancy but increase the chance of SLE.  This cell turnover concept is also useful in understanding the gender differences in the incidences of many other malignancies.
Thank you Mr. Malcom for your contribution, it is deeply appreciated for all to read.
~Kathy

[Adminஐﻬ]

watch this link, watch for Dr Utz. He recently wrote back to Tyler. (I have the email as proof)
There is a TV segment done on ABC news in the San Francisco Bay Area (KGO TV)
http://www.lupus.org/webmodules/webarticlesnet/templates/new_empty.aspx?articleid=1960&zoneid=99

Thanks Tyler!!!

[Adminஐﻬ]

MEET & GREET:
Mr William T. Malcom
To us, he's known as Ty.

Here you will see his work that he had copyrighted back in the early 1980's.

#   Name Heading    Author    Full Title    Date
[ 1 ]    Malcolm, William Tyler, 1958-   

 

   Adolescent bone neoplasms and skeletal growth.    1985
[ 2 ]    Malcolm, William Tyler, 1958-   

 

   Breast carcinomas as uncontrolled menstrual proliferations.    1984
[ 3 ]    Malcolm, William Tyler, 1958-   

 

   CF, C1[superscript]-, and ACE.    1985
[ 4 ]    Malcolm, William Tyler, 1958-   

 

   Complementary biomolecules as potential autoantigens / by William Tyler Malcolm.    1985
[ 5 ]    Malcolm, William Tyler, 1958-   

 

   Neoplasms as uncontrolled regenerative hyperplasia / William Tyler Malcolm.    1984
[ 6 ]    Malcolm, William Tyler, 1958-   

 

   Systemic lupus erythematosus and tissue catabolism / by William Tyler Malcolm.    1985
Then I will provide to you a link to the "Springerlink" on two other people who are researching what Ty copyrighted back in the 1980's called "   Systemic lupus erythematosus and tissue catabolism" (see above and below)


Systemic Lupus Erythematosus and Tissue Catabolism

Copyright 1985 by William Tyler Malcolm

 
A 90% female incidence and a diversity of autoantigens are unusual features of the autoimmune disorder systemic lupus erythematosus (SLE).  The link between estrogenic metabolites and immune stimulation is far too weak to account for SLE's overwhelming female prevalence (besides, any such causal relationship would make all other autoimmune disorders 90% female as well).  The consistent occurrence of the same set of autoantigens and the existence of animal models for SLE suggest that it may be related to a fundamental process.  The immunological aspect of tissue catabolism during necrotic clean up and necrobiotic removal may be this process since most of the autoantigens of SLE are intracellular substances and because female histology is characterized by a high amount of menstrual and pregnancy-related cell turnover in many tissues (endometrium, myometrium, cervical mucus glands, vagina, ovary, mammary epithelia).  Since these processes are driven by sex steroids the studies linking linking these hormones and oral contraceptives to SLE's predisposition or progression make sense when viewed through the steroids' stimulatory or antagonistic effects on the normal hyperplastic processes, rather than through their direct influences on the immune system.  Since tissue catabolism is such a fundamental and certain process it is unlikely that a diverse immune response is generated de novo each time a cell turns over; rather, this complicated response is probably a set of concerted actions narrowly controlled, steadily maintained, and suitably modulated.  The circulating anticoagulants often increased in SLE and the other targets of autoantibody such as platelets, erythrocytes, and lymphocytes fit this hypothesis since one would expect that they function in tissue catabolism, or are normally present at the locus, or are themselves the objects of overly aggressive immune-related turnover mechanisms.  Predictably, complement would function in cell turnover and SLE, unlike most other autoimmune disorders, shows abnormalities in serum complement levels and C3b receptors.  Exposure of the T antigenic determinant (MN blood group precursor) is a possible mechanism of cell turnover.  Humans maintain anti-T IgM even in the absence of disease and females have higher IgM levels than males.  Normally, the T antigen is masked and the pentameric anti-T IgM is inaccessible to tissue cells.  The acidic (trauma environment) or enzymatic unmasking of T followed by its complexing with anti-T IgM at a locus of microtrauma or a site of increased vascular permeability should trigger complement fixation.  It is difficult to imagine why the T antigenic determininant exists and the anti-T IgM is maintained if the resulting complex does not serve some purposeful function, such as initiating cell turnover.  A possible explanation of the reciprocal incidences of breast cancer and SLE between black and white women is that a more active and efficient cell turnover process may reduce the risk of a fully progressed malignancy but increase the chance of SLE.  This cell turnover concept is also useful in understanding the gender differences in the incidences of many other malignancies.
NOW, read the "Springer link" (I can't help but think of Jerry Springer and the nuts he has on his show when I see their URL)
http://www.springerlink.com/content/u5epbu5e0kx2u6b6/
NOTE~ this is NOT an old article from the 1980's, this is present time.As they said back in grade school and with Tyler's copyright "Tyler had first dibs on it!"
KUDOS TYLER, we all believe in you and your copyrights.

[Adminஐﻬ]

Rheumatology Advance Access originally published online on May 31, 2005
SLE—a disease of clearance deficiency?
http://rheumatology.oxfordjournals.org/cgi/content/full/44/9/1101
Notice Tylers date he copywrited his SLE/Tissue  Catabolism, back in the 1980's he had it copyrighted!!! Systemic lupus erythematosus and tissue catabolism / by William Tyler Malcolm 1985

Kudos Tyler   people (scientists/researchers) are just slower ...    Ty you were 20 years ahead of them!!!!

[Adminஐﻬ]

One of many to be posted from Tyler.

PDF file , large, extra large

[Adminஐﻬ]

  Back in 1970 you could catch Tyler doing this...

something not your typical neighborhood boy would do.

 But Tyler was doing it.

Little did we know, that 15 years later Ty would copyright his theory/discovery on SLE/Tissue Catabolism during the time this pic was taken when he became a deep sea diver professionally

The LupusMCTD Foundation of America THANKS you William Tyler Malcom for your contribution towards discovery for us!
People have to understand, you do not have Lupus or a MCTD, and you are the author of 5 other medical copyrights listed in this thread.
KUDOS TYLER!!!
Your'e #1 in our eyes !!!!

THANK YOU!!!! THANK YOU!!!! THANK YOU!!!

[Adminஐﻬ]

If anyone has any questions regarding the SLE/Tissue Catabolism, please send a PM to Tyler
 

[Adminஐﻬ]

[Adminஐﻬ]

[Adminஐﻬ]

SLE/Tissue Catabolism offers a reasonable explanation for the distinct gender imbalance:  Lupus is related to cell turnover, women have more cell turnover than men

http://www.news-leader.com/apps/pbcs.dll/article?AID=/20080908/LIFE04/809080350