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HaPPy 4th of JULY --from PSORiatic - BENJAMIN FRANKLIN - Epigenetics - HDAC Inhibitors -TSA -

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randall

unread,
Jul 3, 2010, 9:43:45 PM7/3/10
to
Hi


History channel had two hours this morning on the LIFE of Ben
Franklin...


Which i saw little of and now regret.

While i tried to listen i didn't hear once about his psoriasis and if
he
even had it.


Which is what this thread is all about.


Let's say he had psor and was....


The GREATEST American perhaPs?


In sPite of his scurfy (psoriasis) Big BEN was a BABE magnet?

[randall note: just like me.. LOL ]

Ben was born on January 17, 1706


and


April 17, 1790 Ben Franklin (BF) passed on.


His persona stands for ALL time...


Ben has been in over 20 posts in the P NG and
mostly quotes at the end of posts.

I'll find a few, but first this next p ng post was full of BF meat:


scrool back one post to get the gist:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/927ab304ba270faf/06400cf046a5b565?hl=en&lnk=gst&q=benjamin+franklin#06400cf046a5b565

to this ( no highlights- so i like the above link better as you can
read a couple of posts)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/f5bfe150b5142bcb


But if you wish not to click then one of two nice hits for BF on the
4th of JULY


http://www.washingtonpost.com/wp-dyn/content/article/2006/01/23/AR2006012301271.html
Of Scabs And Scurf


Notes From a Psoriasis Patient's Journal

By Benjamin Franklin
Special to The Washington Post
Tuesday, January 24, 2006

I first observ'd a kind of Scab or Scurff on my head, about the
Bigness of a Shilling [in the early 1770s]. Finding it did not heal,
but rather increas'd I mention'd it to my Friend Sir J.P. who advis'd
a mercurial Water to wash it, and some Physic. It slowly left that
Place but appear'd in other Parts of my Head.

[In 1776] I went to Canada. On the passage I suffer'd much from a
number of large Boiles. In Canada my Legs swell'd and I apprehended a
Dropsy. Boils continu'd and harrass'd me after my Return, but the
Swelling of my Legs pass'd off. The Boils however left round them a
kind of dry Scab or Scurfiness, which being rubb'd off appear'd in the
Form of white Bran.

. . . In my Passage to France Nov. 1776 I lived chiefly on Salt Beef,
the Fowls being too hard for my Teeth. But being poorly nourish'd, I
was very weak at my Arrival; Boils continu'd to vex me, and the Scurff
extending over all the small of my Back, on my Sides, my Legs, and my
Arms, besides what continued under my Hair, I apply'd to a Physician,
who order'd me Bellosto's Pills and an Infusion of a Root. . . . I
took the Infusion a while, [but] it being disagreable, and finding no
Effect I omitted it. I continu'd longer to take the Pills; but finding
my Teeth loosning and that I had lost 3, I desisted the Use of them.

I found that bathing stop'd the Progress of the Disorder. I therefore
took the Hot Bath twice a Week two Hours at a time till this last
Summer. It always made me feel comfortable, as I rubb'd off the
softned Scurff in the warm Water; and I otherwise enjoy'd exceeding
good Health.

. . . In July the Disorder began to diminish, at first slowly, but
afterwards rapidly; and by the Beginning of October, it had quitted
entirely my Legs Feet Thighs, and Arms, and my Belly, a very little
was left on my Sides, more on the small of my Back, but the whole
daily diminishing. I observ'd that where there was no Redness under
the Scurff, if I took it once off it did not return. I had hardly
bath'd in those 3 Months. I took no Remedy whatever and I know not
what to ascribe the Change to, unless it was the Heat of the Summer,
which sometimes made me sweat, particularly when I exercis'd. I had
five Boiles just before the Amendment commenc'd, which discharged a
great deal of Matter. And once my Legs began to swell.

. . . October 3rd I ate no Breakfast, but a hearty Dinner, and at
Night found my Back itch extreamly near the Shoulders which continues
to day the 4th. I ate some Salted Beef at Dinner yesterday but not
much. I wish the Cool Weather may not bring on a return of the
Disorder.

Oct. 4. The Itching continues, but somewhat abated.

Oct. 6. Drank but one Glass of Wine to day; the Itching almost gone. I
begin to think it will be better for me to abstain from Wine. My
Dinner to day was Mutton boil'd and Fowl, with a good deal of Fruit.

Oct. 12. I have lately drank but little Wine. The Itching has not
return'd. The Scurff continues to diminish. But yesterday I observ'd
my Ancles swell'd. I suppose my having us'd no Exercise lately may be
the Cause.

Jan. 14, 1779. The Swelling above mention'd continu'd some few Weeks,
being greatest at Night, my Complexion at the same time not fresh; at
length the Itching return'd, and a new Set of Eruptions of scurfy
Spots appear'd in many Parts of my Body. My Back had never been
entirely clear'd and the Scurf began to increase there and extend
itself. But it is not yet so bad as it has been, and it seems to spare
the parts that were before affected, except in my Back. The Swelling
has left my Legs, which are now as dry and firm as ever, and I feel
myself otherwise on perfect health, and have as much Vigour and
Activity as can be expected at my Age. So that I begin to be more
reconcil'd to this troublesome disorder, as considering it an Effort
of nature to get rid of Peccant Matter, that might if not so
discharg'd, break up my Constitution.

. . . Jan. 16, 1780. I have enjoy'd good Health ever since the last
Date. Towards the End of the Summer most of the Disorder in my Skin
disappeared, a little only remaining on my left Arm, a little under
each Breast, and some on the small of the Back. I had taken at
different times a good deal of Dr. Pringle's Prescription; but whether
that occasion'd the Amendment, or whether it was the Heat of the
Summer as I suppos'd in October 1778, I am uncertain. The disorder
seems to be now increasing again, and appears upon my hands. I am
otherwise well; my Legs sound; To-morrow I enter my 75th Year. ·

Benjamin Franklin was an architect of U.S. democracy, a diplomat, an
inventor and a psoriasis patient. These excerpts are adapted from his
writings about the skin condition, appearing in "The Papers of
Benjamin Franklin" (Oct. 14, 1778 through Jan. 16, 1780). The writings
were assembled by Mike Paranzino, president of Psoriasis Cure Now!, a
Kensington-based nonprofit group to mark the 300th anniversary of
Franklin's birth. Paranzino said he wants people know that the
incurable skin condition affects many productive, accomplished people
-- and to demonstrate how little has changed for psoriasis patients in
300 years. For information on psoriasis conditions and treatment:
www.psorcurenow.org.

--------


Whoops gave psorcure a booster shot. LOL

So? Special thanks to Michael Paranzino (psoriasis cure now) as we
have his notes (above) right here:
http://www.psoriasis-cure-now.org/benfranklin-psoriasiswritings.php


[The above wahington post story doesn't have this info]

[...]
-------------------

Franklin’s Description of His Ailments3
Oct. 17, 17774
"The Papers of Benjamin Franklin," Vol. 25, pages 77-80.
Yale University Press.


[Franklin wrote this account in the third person, as it was to be
taken by a friend of Franklin to London to get an expert’s opinion
about treatment.]

… About 3 Years since he found a small Spot on his Head cover’d with a
dry Scurff, which when rubb’d off from time to time, left always a
Moisture on the Part that form’s another Scurf. This continuing some
Months, and seeming to extend itself, alarm’d him, and he consulted
Sir J.P. who prescrib’d a Water to wet the Part, and some Pills, which
Prescription was follow’d, and the Disorder by slow Degrees quitted
that Spot, but after some time show’d itself in other Parts of the
Head.

The greatest Part of the Year 1775 he was almost every day 10 or 12
hours of

the Day employ’d in Business of Consultation with many other Persons
sitting in a close Room, and had no Leisure for Exercise. During this
time the Disorder spread, and affected his Head in a Number of small
Spots under the Hair, the Scurf tho’ taken off from time to time by
the Comb, returning continually. …

[Some people believe Franklin took to wearing this hat to cover up his
head psoriasis.]

Towards the End of Winter 1776, he set out on a Journey of 500 Miles,
of which great Part was perform’d in a small open Boat, where he was
kept sitting without Exercise for many Days. During this Journey which
continu’d from the Middle of March to the Beginning of June, he was
afflicted with a Succession of Boils, sometimes two or three together,
each when heal’d leaving round about it Spots of the same Scurff,
which obstinately continu’d, being renew’d after every Removal. At
this time his legs swell’d in the Small, and Impressions made by the
Finger would continue long. This Swelling went away on his Return
home, but the Boils continu’d to harass him.

In November 1776 he made a long Sea Voyage, in which the Disorder
sensibly increas’d, and the Boils became more frequent. Part of each
Arm, and of each side, the Small of his Back, and Parts of his Thighs
and Legs, became cover’d with the Scurff, which became very
troublesome, itching sometimes extremely, and when rubb’d or scratch’d
off, would spot his Linen with Blood.

He consulted a Physician, who prescribed Belloste’s Pills, and an
Infusion of a Root called Patience, or the Rhubarb of the Parisians.
This Prescription was followed some time, till the Mouth began to have
an unusual Quantity of Water in it, and the Teeth to be a little
loosened. The Disorder was not diminished, but appeared not to
increase.

He has for sometime omitted taking those Pills,5 but uses the warm
Bath twice a Week, staying in the Water each time near two Hours,
which are employ’d in rubbing off the Surff when softened by the
Water, and so clearing the Skin. The Disorder has now visibly
diminish’d; for in many Places after the Scurff has thus been
repeatedly rubb’d off, it does not return, leaving the Skin soft and
natural. But the Amendment is slow; and it is apprehended, that on a
Discontinuance of the bathing, it may return and increase as before.

The Scurf appears to be compos’d of extreamly thin Scales one upon
another, which are white, and when rubb’d off dry, are light as Bran.
When the Skin is clear’d in the Bath, it looks red, and seems a little
elevated above the sound Skin that is around the Place; but it is not
sore: And in a few Hours after, it becomes dry, and feels stiffned
even in warm Water. The fine Lamina seem to be formed one under
another, and not to make an united thick Substance by adhering
together. In rubbing them off they separate, like Talc, each having a
Polish that shines.

His Head is now almost clear of the Disorder, as are also his Legs and
Thighs, and it seems diminish’d on his Arms. But it holds it s ground
on the Small of his Back and his Side.

There were in the Heighth of it some small Spots on his Hands and
Face, but they have quite disappear’d.

... He wishes to be inform’d Whether this troublesome Disease may not
be of Service to him in other Respects?

Whether it be safe to cure it?

If so, what are the medicines to be used?

And what ought to be his Regimen?

Endorsed: Dr Franklin’s case written by him, and consulting me upon
it.
<haven't a clue? neither do i. LOL -- psor- randall>

-------

News Release Announcing Psoriasis Cure Now's Ben Franklin Campaign

http://www.psoriasis-cure-now.org/011606ben.php

---

Ben Franklin & Psoriasis: Little Has Changed Since Franklin's Time
http://www.psoriasis-cure-now.org/franklin-psoriasis.php


------------


Lets find some Ben Franklin quotes from the P NG:


---

ZipPo posted this quote a few times:

"They that can give up essential liberty to obtain a little temporary
safety deserve neither liberty nor safety."


Benjamin Franklin

-----------


Olive eye posted this:

1998/05/05
Subject: For Lovers of Law & Order & more.
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/3b167dcf72b9a826

[...]
Comin's Law:
People will accept your idea much more readily if you tell them
Benjamin
Franklin said it first.

<sniP>

-----------

Chuck (URAQT2) posted this:


There has never been a good war or a bad peace.-Benjamin Franklin


----------

More BEN?


Yes...

YKW posted this here:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/bc9734c49ace944c

A book about ben?

But this next link doesn't work. (so don't USE it. LOL)
http://www.google.com/url?sa=D&q=http://www.americanscientist.org/template/BookReviewTypeDetail/assetid/53125%3Bjsessionid%3Dbaa8kAxfcQiRf3&usg=AFQjCNE_IVMS3arey8hVqMPc7J4hb5xheA

Reflected Light?
Barry W. Allen (PhD --Anesthesiology )


Doctor Franklin's Medicine. Stanley Finger. xiv + 379 pp. University
of
Pennsylvania Press, 2006. $39.95.


Few personalities swept a more luminous arc through 18th-century
America than did Benjamin Franklin. An autodidact, polymath, patriot
and successful businessman, he was wealthy enough at the age of 42 to
retire from commerce and devote the rest of life to philanthropy,
diplomacy and science. Among many achievements, he may have been the
first to have the powerful insight that the various manifestations of
electricity are a single phenomenon best understood as a kind of
fluid.


Franklin's celebrity was due to his formidable intelligence,
unparalleled energy and admirable assiduity, and also to
circumstance:
He owned a printing press, and his literary alter ego, Poor Richard,
had something to say about almost everything of interest to a broad,
Colonial audience.


Franklin also actively sought fame, and some of his renown was
self-created: He dissimulated humility while inwardly belittling it.
"I
cannot boast of much Success in acquiring the Reality of this Virtue,
but I had a good deal with regard to the Appearance of it," he wrote
candidly in his Autobiography. He smoothly ingratiated himself with
many of the best thinkers and doers of his time, without seeming to
try, but trying all the while, especially in his younger years. To
gain
the attention or favor of someone important, he suggested, one should
ask to borrow a book from that person's library-a marvelously
disingenuous method of flattering even the most wary. He also
counseled
that older mistresses are to be preferred because they are so much
more
grateful.

The remainder of the book is organized chronologically and by
scientific discipline. Finger describes Franklin's contributions to
the
emerging recognition of the health benefits of exercise and fresh
air,
the promotion of inoculation against smallpox, the establishment in
America of the first hospital and then the first medical school, the
formation of scientific and medical societies, the understanding of
airborne contagion and lead poisoning, the resolution of the struggle
between theorists and pragmatists in medicine, and advocacy for the
therapeutic role of music. The last chapters deal with Franklin's
more
intimate connection to medical conditions from which he personally
suffered: presbyopia, gout, a chronic skin disease (presumably
___psoriasis__) and bladder stones.
<sniP>


OK so i had to find more of this.

And did here:


http://www.americanscientist.org/bookshelf/pub/reflected-light

[...]
We see Franklin develop through his own experience a sobering
appreciation of the limits of medicine.

As Finger conducts this fascinating tour of medical history, he
enlivens the narrative with information that is often useful and
always interesting. What does the word "inoculation" have to do with
the eye? What is "small" about smallpox? Why is gout so named?
Numerous other fascinating anecdotes and little histories demonstrate
a broad scholarship and an eclectic passion for knowledge. The book's
extensive endnotes facilitate entry into both the primary literature
of Franklin studies and the intellectual history of his time.

Doctor Franklin's Medicine is a valuable and entertaining work.
However, Finger wisely concedes in his preface that this is not a
definitive book on Franklin's contributions to medicine; he hopes
others will undertake that project. I hope so too.

Franklin's dazzling career has led to the creation of an apparently
solid edifice, which no doubt conceals some element of myth, and my
only quibble with the book's assessment of Franklin's contributions to
medicine is that it may not be critical enough. Finger does not dwell
on the complexity of his subject's character and generally takes the
Franklin mythology at face value. For example, did Franklin
independently invent (or reinvent) the blind protocol that is so
important to modern scientific method? Or was the protocol the
contribution of Antoine Lavoisier, the even more brilliant father of
modern chemistry, who served with Franklin on the committee that
helped to debunk Mesmerism? The latter may be true, but as Finger
points out, Franklin's signature appears above those of his colleagues
on the final report. One would have to dig deep to find the truth.

Franklin the scientist deserves further scholarly scrutiny, not to
diminish him but to reveal the man as he was. Within the past decade
or so, a number of authors have begun to demythologize that other
meteor of the 18th-century American firmament, Thomas Jefferson. I
hope someone will follow Finger's advice and untangle the multiple
strands of Franklin's contributions to the development of scientific
medicine. Was he an innovator or a popularizer? A scientist or a
gifted enthusiast? I expect he was some of each.

Franklin's brilliance is unquestioned, but how much of it is reflected
light?
<sniP>


OK let's find this book that sounds like a real trip to psor ben?


Right ON... GEE...


Doctor Franklin's Medicine. Stanley Finger (checking amazon)

Caught it:
http://www.amazon.com/Doctor-Franklins-Medicine-Stanley-Finger/dp/081223913X


===================


And we have daveW's psorsite and famous people:

http://www.psorsite.com/famous.html

Famous People with Psoriasis
A list of some famous and infamous people with psoriasis, or maybe
just suspected of having psoriasis.

<sniP>


A good site:
http://www.psorsite.com/sitemap.html

But i don't see anything directly for Benjamin Franklin in Dave's
famous people with psoriasis page.

We have stalin and updike and stars and such.


============

A person on this next forum mentions Benjamin Franklin.

Lala say so said:

http://www.davidicke.com/forum/showthread.php?t=55260

[...]

Theory: The Heartbreak of Psoriasis = Reptilian Ancestors


I came up with this theory after someone posted on a Psoriasis Forum
“I feel like one of those David Ike lizard-people”.

[...]
People with Psoriasis Live Longer {and lala says are smarter and need
sunlight et al}

Psoriasis suffers have higher Uric Acid levels(20-30% higher) than
individuals without Psoriasis.

Various studies show that high levels of uric acid are transferred
genetically, just like psoriasis itself. And even those people with
psoriasis, who do not have any external psoriasis manifestations (i.e.
the so-called latent psoriasis), also have high levels of Uric Acid in
their bodies. With the elimination of the psoriatic plaques on the
skin under the effect of, for example, UVB therapy, the levels of the
uric acid in the body stay the same as they were before the
elimination of the psoriatic lesions.

Uric acid helps to lower the cell's oxidation and thus helps to slow
the body tissue aging. This all is achieved by the protection against
the free radicals and their damage, provided by the uric acid.
Slower body tissue aging will clearly result in the prolonged lifespan
of the whole body.

People with Psoriasis Are Smarter


High levels of Uric Acid may ensure higher Intellectual and Physical
Activity in the people with psoriasis, compared to the people without
psoriasis.
Therefore the people with psoriasis may be smarter and have a better
physical make-up than the people without psoriasis.
<sniP>


=============


ON this day, July 3rd, 2010 we get 1,580 hits for keywords: Benjamin
Franklin on google NEWs
http://www.google.com/webhp?hl=en&tab=gw#hl=en&q=benjamin%20franklin&um=1&ie=UTF-8&tbo=u&tbs=nws:1&source=og&sa=N&tab=wn&fp=4f24dd8c1ebe2db1


Do we ever get that many for psoriasis?

NO.... we run between 150 and 450 hits at any given time...

Right now if you substitute psoriasis for ben franklin you get 401
hits.

You get zero hits for keywords: benjamin franklin psoriasis on google
news.


Maybe if Ben had lived another 300 years he'd have found a cure for
psoriasis?


Or at least a better way to live with a life time of psor?


BF never heard of epigenetics. (75 hits on google news)

http://www.google.com/webhp?hl=en&tab=gw#hl=en&tbo=p&tbs=nws%3A1&q=epigenetics&aq=f&aqi=g1&aql=&oq=&gs_rfai=&fp=affe369ed90cb79


This one looks good

http://blogs.discovermagazine.com/loom/2010/06/17/epigenetics-and-the-brain-woo-free-coolness/

http://discovermagazine.com/2010/jun/15-brain-switches-that-can-turn-mental-illness-on-off/article_view?b_start:int=0&-C=
http://discovermagazine.com/2010/jun/15-brain-switches-that-can-turn-mental-illness-on-off/article_view?b_start:int=1&-C=

Hey the second page has HdAC inhibitors and that is a psor thing to
clear up some.


i'll run this thing.

Maybe BF would be doing HDAC inhibitors and hanging with the bABEs
right now?


<link is www.discovermagazine.com right up a few lines>
The Brain The Switches That Can Turn Mental Illness On and Off

The difference between one personality and another is not determined
by genes alone. Love’s got something to do with it too.

by Carl Zimmer

This month’s column is a tale of two rats. One rat got lots of
attention from its mother when it was young; she licked its fur many
times a day. The other rat had a different experience. Its mother
hardly licked its fur at all. The two rats grew up and turned out to
be very different. The neglected rat was easily startled by noises. It
was reluctant to explore new places. When it experienced stress, it
churned out lots of hormones. Meanwhile, the rat that had gotten more
attention from its mother was not so easily startled, was more
curious, and did not suffer surges of stress hormones.

The same basic tale has repeated itself hundreds of times in a number
of labs. The experiences rats had when they were young altered their
behavior as adults. We all intuit that this holds true for people,
too, if you replace fur-licking with school, television, family
troubles, and all the other experiences that children have. But
there’s a major puzzle lurking underneath this seemingly obvious fact
of life. Our brains develop according to a recipe encoded in our
genes. Each of our brain cells contains the same set of genes we were
born with and uses those genes to build proteins and other molecules
throughout its life. The sequence of DNA in those genes is pretty much
fixed. For experiences to produce long-term changes in how we behave,
they must be somehow able to reach into our brains and alter how those
genes work.

Neuroscientists are now mapping that mechanism. Our experiences don’t
actually rewrite the genes in our brains, it seems, but they can do
something almost as powerful. Glued to our DNA are thousands of
molecules that shut some genes off and allow other genes to be active.
Our experiences can physically rearrange the pattern of those switches
and, in the process, change the way our brain cells work. This
research has a truly exciting implication: It may be possible to
rearrange that pattern ourselves and thereby relieve people of
psychiatric disorders like severe anxiety and depression. In fact,
scientists are already easing those symptoms in mice.


Two families of molecules perform that kind of genetic regulation. One
family consists of methyl groups, molecular caps made of carbon and
hydrogen. A string of methyl groups attached to a gene can prevent a
cell from reading its DNA sequence. As a result, the cell can’t
produce proteins or other molecules from that particular gene. The
other family is made up of coiling proteins, molecules that wrap DNA
into spools. By tightening the spools, these proteins can hide certain
genes; by relaxing the spools, they can allow genes to become active.

Together the methyl groups and coiling proteins—what scientists call
the epigenome—are essential for the brain to become a brain in the
first place. An embryo starts out as a tiny clump of identical stem
cells. As the cells divide, they all inherit the same genes but their
epigenetic marks change. As division continues, the cells pass down
not only their genes but their epigenetic marks on those genes. Each
cell’s particular combination of active and silent genes helps
determine what kind of tissue it will give rise to—liver, heart,
brain, and so on. Epigenetic marks are remarkably durable, which is
why you don’t wake up to find that your brain has started to turn into
a pancreas.

Our experiences can rewrite the epigenetic code, however, and these
experiences can start even before we’re born. In order to lay down the
proper pattern of epigenetic marks, for example, embryos need to get
the raw ingredients from their mothers. One crucial ingredient is a
nutrient called folate, found in many foods. If mothers don’t get
enough folate, their unborn children may lay down an impaired pattern
of epigenetic marks that causes their genes to malfunction. These
mistaken marks might lead to spina bifida, a disease in which the
spinal column fails to form completely.

Other chemicals can interfere with epigenetic marks in embryos. Last
year, Feng C. Zhou of Indiana University found that when pregnant lab
rats consumed a lot of alcohol, the epigenetic marks on their embryos
changed dramatically. As a result, genes in their brains switched on
and off in an abnormal pattern. Zhou suspects that this rewriting of
the epigenetic code is what causes the devastating symptoms of fetal
alcohol syndrome, which is associated with low IQ and behavioral
problems.

Even after birth the epigenetic marks in the brain can change. Over
the past decade, Michael Meaney, a neurobiologist at McGill
University, and his colleagues have been producing one of the most
detailed studies of how experience can reprogram the brain’s genes.
They are discovering the molecular basis for the tale of the two rats.

The differences between rats that got licked a lot and those that got
licked only a little do not emerge from differences in their genes.
Meaney found that out in an experiment involving newborn rat pups. He
took pups whose mothers who didn’t lick much and placed them with
foster mothers who licked a lot, and vice versa. The pups’ experience
with their foster mothers—not the genes they inherited from their
biological mothers—determined their personality as adults.

To figure out how licking had altered the rats, Meaney and his
colleagues looked closely at the animals’ brains. They discovered
major differences in the rats’ hippocampus, a part of the brain that
helps organize memories. Neurons in the hippocampus regulate the
response to stress hormones by making special receptors. When the
receptors grab a hormone, the neurons respond by pumping out proteins
that trigger a cascade of reactions. These reactions ripple through
the brain and reach the adrenal glands, putting a brake on the
production of stress hormones.

In order to make the hormone receptors, though, the hippocampus must
first receive signals. Those signals switch on a series of genes,
which finally cause neurons in the hippocampus to build the receptors.
Meaney and his colleagues discovered something unusual in one of these
genes, known as the glucocorticoid receptor gene: The stretch of DNA
that serves as the switch for this gene was different in the rats that
got a lot of licks, compared with the ones that did not. In the rats
without much licking, the switch for the glucocorticoid receptor gene
was capped by methyl groups, and the neurons in the underlicked rats
did not produce as many receptors. The hippocampus neurons therefore
were less sensitive to stress hormones and were less able to tamp down
the animal’s stress response. As a result, the underlicked rats were
permanently stressed out.

These studies hint at how experiences in youth can rewrite the
epigenetic marks in our brains, altering our behavior as adults.
Meaney and his colleagues cannot test this hypothesis by running
similar experiments on humans, of course, but last year they published
a study that came pretty close.

Meaney’s team examined 36 human brains taken from cadavers. Twelve of
the brains came from people who had committed suicide and had a
history of abuse as children. Another 12 had committed suicide without
any such history. The final 12 had died of natural causes. The
scientists zeroed in on the cells from the hippocampi of the cadavers,
examining the switch for the stress hormone gene they had studied in
rats. Meaney and his colleagues found that the brains of people who
had experienced child abuse had relatively more methyl groups capping
the switch, just as the researchers had seen in rats that had not been
licked much as pups. And just as those rats produced fewer receptors
for stress hormones, the neurons of the people who had suffered child
abuse had fewer receptors as well.

Child abuse may leave a mark on its victims in much the same way that
parental neglect affects rat pups. Abuse seems to have altered the
epigenetic marks in their hippocampi. As a result, they made fewer
stress receptors on their neurons, which left them unable to regulate
their stress hormones, leading to a life of anxiety. That extra stress
may have played a part in their committing suicide.

The hippocampus is probably not the only place where experiences
rewrite epigenetic marks in the brain. An international group of
researchers recently compared the brains of 44 people who had
committed suicide with those of 33 people who died of natural causes.
The scientists looked at a gene that produces the protein BDNF, which
promotes hormone receptors, in a part of the brain called the Wernicke
area. That area, located behind the left ear in most people, helps us
interpret the meanings of words. In March the researchers reported
that the BDNF switch had more methyl groups attached to it in the
Wernicke area of suicide victims than in other people.

And the influence of environment doesn’t end with childhood. Recent
work indicates that adult experiences can also rearrange epigenetic
marks in the brain and thereby change our behavior. Depression, for
example, may be in many ways an epigenetic disease. Several groups of
scientists have mimicked human depression in mice by pitting the
animals against each other. If a mouse loses a series of fights
against dominant rivals, its personality shifts. It shies away from
contact with other mice and moves around less. When the mice are given
access to a machine that lets them administer cocaine to themselves,
the defeated mice take more of it.

Eric Nestler, a neuroscientist at Mount Sinai School of Medicine in
New York City, wondered what the brains of these depressed mice looked
like. Last fall he reported discovering an important difference in a
region of the brain called the nucleus accumbens. It was probably no
coincidence that depression altered this region, since the nucleus
accumbens plays an important role in the brain’s reward system,
helping to set the value we put on things and the pleasure we get from
them.

The change Nestler and his colleagues discovered in the nucleus
accumbens was epigenetic: Some of the DNA in the neurons in that
region became more tightly or less tightly wound in depressed mice.
Such an epigenetic change might permanently alter which genes are
active in the brains of those mice. The same may hold true for humans.
Nestler’s team looked at cadaver brains from people who had been
diagnosed with depression in life. They discovered the same epigenetic
changes in the human nucleus accumbens.

If scientists can pinpoint the epigenetic changes that our experiences
impart, it may be possible to reverse those changes. Nestler and his
colleagues pumped drugs known as ____HDAC inhibitors____ into the
nucleus accumbens of their depressed mice. These drugs can loosen
tight spools of DNA, making it possible for cells to gain access to
genes again. Ten days after treatment, the mice were more willing to
approach other mice. The drug also erased many other symptoms of
depression in the animals.

The possibility that we can rewrite the epigenetic code in our brains
may be exciting, but it is also daunting. Modifying epigenetic markers
is not easy—and that’s a good thing. After all, if our methyl groups
and coiling proteins were constantly shifting, depression would be the
least of our problems. Nothing ruins your day like finding that your
brain has turned into a pancreas.
<sniP.


Here's the link for HDAC inhibitors:
http://www.hdacis.com/


And the psoriasis hoPe for hdac's


http://www.ncbi.nlm.nih.gov/pubmed/20583972
Curr Drug Targets. 2010 Jun 28.

Histone Deacetylase Inhibitors: New Promise in the Treatment of Immune
and Inflammatory Diseases.
Shuttleworth SJ, Bailey SG, Townsend PA.

Karus Therapeutics Ltd, Southampton Science Park, Southampton, SO16
7NP, UK. P.A.To...@southampton.ac.uk.

Abstract
The development of Histone Deacetylase (HDAC) inhibitors has, until
recently, principally been driven by their potential as anti-cancer
agents. However, there is emerging evidence that HDAC inhibitors could
have utility in the treatment of chronic immune and inflammatory
disorders, including rheumatoid arthritis, psoriasis, inflammatory
bowel disease, multiple sclerosis, systemic lupus erythematosus,
airway hyperresponsiveness and organ transplant rejection. Here we
discuss the merits of various, structurally-distinct HDAC inhibitors
as potential anti-inflammatory therapeutics and provide examples of
the novel medicinal chemistry approaches being undertaken to realize
HDAC as a druggable target in this clinical setting.

PMID: 20583972


353 hits - hdac AND epigenetic - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=hdac+epigenetic


Only one of these has the kicker term: Th17

Use TSA to knock back Th17?

iirc we've posted this one.


Blood. 2008 Sep 15;112(6):2340-52. Epub 2008 Jul 10.

Human CD25highFoxp3pos regulatory T cells differentiate into IL-17-
producing cells.
Koenen HJ, Smeets RL, Vink PM, van Rijssen E, Boots AM, Joosten I.

Department of Blood Transfusion and Transplantation Immunology,
Radboud University Nijmegen Medical Centre, The Netherlands.
h.ko...@abti.umcn.nl

Abstract
The effector T-cell lineage shows great plasticity. Th17 cells are
acknowledged to be instrumental in the response against microbial
infection, but are also associated with autoimmune inflammatory
processes. Here, we report that human regulatory T cells
(CD4(pos)CD25(high)Foxp3(pos)CD127(neg)CD27(pos)) can differentiate
into IL-17-producing cells, when stimulated by allogeneic antigen-
presenting cells, especially monocytes, in the presence of rhIL-2/
rhIL-15. These regulatory T cell (Treg)-derived IL-17-producing cells
showed high expression of the Th17-related transcription factor
RORgammat and were positively identified by CCR6 expression. This
differentiation process was enhanced by exogenous IL-1beta, IL-23, and
IL-21, whereas IL-6 or TGFbeta did not affect the emergence of IL-17-
producing cells. The addition of IL-1 receptor antagonist (IL-1Ra),
but not anti-IL-23 antibody, reduced IL-17-producing cell numbers.
When an histone deacetylase (HDAC) inhibitor trichostatin A (TSA) was
evaluated, we found a profound negative effect on the emergence of
IL-17-producing cells from Tregs, implying that Treg differentiation
into IL-17-producing cells depends on histone/protein deacetylase
activity. Thus, the data suggest that epigenetic modification
underlies the phenomenon of Treg plasticity here described.

PMID: 18617638


Yep, it was posted at the time.

http://groups.google.com/groups/search?hl=en&qt_s=1&q=PMID%3A+18617638

to

Mon, Jul 21 2008 12:06 am
Subject: Re: Endocrine-Immune Mechanisms
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/fb075d038dddb82a

=============


http://www.ncbi.nlm.nih.gov/pubmed/20596736
Amino Acids. 2010 Jul 2.

Novel S100A7 (psoriasin)/S100A15 (koebnerisin) subfamily: highly
homologous but distinct in regulation and function.
Wolf R, Ruzicka T, Yuspa SH.

Laboratory of Cancer Biology and Genetics, Center for Cancer Research,
National Cancer Institute, Bethesda, MD, USA, Ronal...@med.uni-
muenchen.de.

Abstract
S100A7 (psoriasin) and S100A15 (koebnerisin) were first identified in
inflamed psoriatic skin. They are of major interest because of their
putative functional roles in innate immunity, epidermal cell
maturation, and epithelial tumorigenesis. Human S100A7 and S100A15
have lately evolved by gene duplications within the epidermal
differentiation complex (chromosome 1q21) during primate evolution
forming a novel S100 subfamily. Therefore, S100A7 and S100A15 are
almost identical in sequence (>90%) and are difficult to discriminate.
Despite their high homology, S100A7 and S100A15 are distinct in tissue
distribution, regulation, and function, and thus, exemplary for the
diversity within the S100 family. Their different properties are
compelling reasons to discriminate S100A7 (psoriasin) and S100A15
(koebnerisin) in epithelial homeostasis, inflammation, and cancer.

PMID: 20596736

-----

http://www.ncbi.nlm.nih.gov/pubmed/20594301
J Biomed Sci. 2010 Jul 1;17(1):53. [Epub ahead of print]

Regulation of cytokines by small RNAs during skin inflammation.
Bak RO, Mikkelsen JG.

Abstract
ABSTRACT: Intercellular signaling by cytokines is a vital feature of
the innate immune system. In skin, an inflammatory response is
mediated by cytokines and an entwined network of cellular
communication between T-cells and epidermal keratinocytes.
Dysregulated cytokine production, orchestrated by activated T-cells
homing to the skin, is believed to be the main cause of psoriasis, a
common inflammatory skin disorder. Cytokines are heavily regulated at
the transcriptional level but emerging evidence suggests that
regulatory mechanisms that operate after transcription play a key role
in balancing the production of cytokines. We review here the nature of
cytokine signaling in psoriasis with particular emphasis on regulation
by mRNA destabilizing elements and the potential targeting of cytokine-
encoding mRNAs by miRNAs. The proposed linkage between mRNA decay
mediated by AU-rich elements and miRNA association is described and
discussed as a potential general feature of cytokine regulation in
skin. Moreover, we describe the latest attempts to therapeutically
target cytokines at the RNA level in psoriasis by exploiting the
cellular RNA interference machinery. The applicability of cytokine-
encoding mRNAs as future clinical drug targets is evaluated, and
advances and obstacles related to topical administration of RNA-based
drugs targeting the cytokine circuit in psoriasis are described.

PMID: 20594301

"Mikkelsen JG"[Author] 26 studies
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mikkelsen%20JG%22%5BAuthor%5D

==================

HAVE a HaPPy 4 th of JULY


Don't let anything get you DOWN...


randall....

JRStern

unread,
Jul 6, 2010, 5:56:47 PM7/6/10
to
On Sat, 3 Jul 2010 18:43:45 -0700 (PDT), randall <ranh...@aol.com>
wrote:

>The last chapters deal with Franklin's more
>intimate connection to medical conditions from which he personally
>suffered: presbyopia, gout, a chronic skin disease (presumably
>___psoriasis__) and bladder stones.


well, my right foot now says I have *two* things in common with ol'
Ben.

J.

randall

unread,
Jul 9, 2010, 6:14:07 PM7/9/10
to
On Jul 6, 2:56 pm, JRStern <JRSt...@foobar.invalid> wrote:
> On Sat, 3 Jul 2010 18:43:45 -0700 (PDT), randall <ranhu...@aol.com>

> wrote:
>
> >The last chapters deal with Franklin's more
> >intimate connection to medical conditions from which he personally
> >suffered: presbyopia, gout, a chronic skin disease (presumably
> >___psoriasis__) and bladder stones.
>
> well, my right foot now says I have *two* things in common with ol'
> Ben.
>
> J.

J,


Not really. LOL

It says:

***In 1776] I went to Canada. On the passage I suffer'd much from a


number of large Boiles. In Canada my Legs swell'd and I apprehended a
Dropsy. Boils continu'd and harrass'd me after my Return, but the
Swelling of my Legs pass'd off. The Boils however left round them a
kind of dry Scab or Scurfiness, which being rubb'd off appear'd in
the

Form of white Bran.****


If this is Ben's onset----> look at the DATE. -----> 1776

That was ONE HELL of a YEAR no doubt.

http://en.wikipedia.org/wiki/1776

And look again at when ben was born:

**Ben was born on January 17, 1706 **


BEN onset with white brain looking scurf (psoriasis?) at the age of
70.

<he only lived another 14 years>

If you live to 84 then you'll have something in common. But you'll
have to live in to your 100's to be cured and live as long as BEN
did without scurf. That's an odd way to look at it?

But the GLASS is half full. LOL

I'm fairly sure if he was, and it seems MOST likely that BEN
was, a BABE magnet, that he didn't give a flying fig about bran
flakes on his legs by the age of 70.

But who knows for absolute positive?

I can speculate uPon empirical puddings close to home perhaps?

Two of the folks in my immediate family who onset at nearly 50 y/o
never gave a rats behind about their scurf either.

And they and i are ALL BABE magnets for the record.

So we have that in common. LOL

It's a rough road to hoe but someone has too...

The only diff being i was an early ONSET.

I had scurf when i learned to surf.

Luckily the sun and vitamin D3 (sunshine) days seemingly
was the only topical i needed till my late teens or so.

I quickly gave up the tar topical as it made me smell funny.

And surely NO babe magnet smells like a TAR baby. LOL

I wonder how long it would take for me to live as long
as ben did without scurf.

Let's see, i'd have to live another 64 years.

They better figure out how to slow the decay of telomere's pronto.

120 years old isn't enough. I'd have to clear now and then stay clear
till 122 like Jeanne
Calment. But she was 121 1/2 wasn't she?

I don't know... do a post on her again. It's like i've only mentioned
her a 100 times. LOL

Can we live past 120 and what does the hayflick limit say about DAT?

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

http://en.wikipedia.org/wiki/Telomere
A telomere is a region of repetitive DNA at the end of a chromosome,
which protects the end of the chromosome from deterioration. Its name
is derived from the Greek nouns telos (τἐλος) "end" and merοs (μέρος,
root: μερ-) "part".

Russian theorist Alexei Olovnikov was the first to recognize (1971)
the problem of how chromosomes could replicate right to the tip, as
such was impossible with replication in a 5' to 3' direction. To solve
this and to accommodate Leonard Hayflick's idea of limited somatic
cell division, Olovnikov suggested that DNA sequences would be lost in
every replicative phase until they reached a critical level, at which
point cell division would stop.[1][2]

During cell division, enzymes that duplicate the chromosome and its
DNA cannot continue their duplication all the way to the end of the
chromosome. If cells divided without telomeres, they would lose the
ends of their chromosomes, and the necessary information they contain.
(In 1972, James Watson named this phenomenon the "end replication
problem".) The telomeres are disposable buffers blocking the ends of
the chromosomes and are consumed during cell division and replenished
by an enzyme, the telomerase reverse transcriptase.

They have been likened to the aglets (tips) on the ends of shoelaces
that keep them from fraying.[3]

In 1975–1977, Elizabeth Blackburn, working as a postdoctoral fellow at
Yale University with Joseph Gall, discovered the unusual nature of
telomeres, with their simple repeated DNA sequences composing
chromosome ends. Their work was published in 1978. The telomere
shortening mechanism normally limits cells to a fixed number of
divisions, and animal studies suggest that this is responsible for
aging on the cellular level and sets a limit on lifespans. Telomeres
protect a cell's chromosomes from fusing with each other or rearranging
—abnormalities which can lead to cancer—and so cells are normally
destroyed when their telomeres are consumed. Most cancers are the
result of "immortal" cells which have ways of evading this programmed
destruction.[4]

Elizabeth Blackburn, Carol Greider, and Jack Szostak were awarded the
2009 Nobel Prize in Physiology or Medicine for the discovery of how
chromosomes are protected by telomeres and the enzyme telomerase.[5]
<sniP>

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

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

I wonder how telomerase and microRNA interact?

And i wonder if cancer is compensatory for the hayflick limit?

http://en.wikipedia.org/wiki/Telomerase#Cancer


One thing is for sure it's different between men and women.

And aging isn't an easy topic.

http://en.wikipedia.org/wiki/Telomerase#Aging


BENJAMIN FRANKLIN certainly lived a FULL life in his 84
years.

I saw the movie the LAST STATION (end of the line for leo tolstoy)
recently and loved it.
http://en.wikipedia.org/wiki/The_Last_Station

Tolstoy lived 82 years

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

==================


But last week was i saw an article about a post office worker
who retired at the age of 94 iirc.

And he seemed really kewl...


I'll do a post and include HIM and Jeanne Calment soon. :)


Let's see take NAC, ALA, ALC or alcar and all the other goodies.

And get the right microRNA's and and and... exercise.... and...


randall...I'd be happy as BEN if i onset in another decade or so plus
change. LOL

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