Re: Informative vit D article
JRStern
>x-no-archive: yes
>
>http://www.ft.com/cms/s/2/11180df8-beaa-11de-b4ab-00144feab49a.html
good article ... in ft? whatever.
FTA:
Can we overdose?
One of the debates surrounding vitamin D is whether too much can be
toxic. The US�s Institute of Medicine�s recommendations � unchanged
since 1997 � were influenced in part by a 1984 study concluding that
3,800 IU of vitamin D per day could cause hypercalcemia, or too much
calcium in the blood. Symptoms include kidney stones, vomiting and
muscle atrophy.
But the 1984 study was flawed: it failed to measure the amount of
vitamin D administered; based on the findings of other studies, it now
looks as though subjects were given 100 times more vitamin D than
intended.Moreover, how could it be that 3,800 IU was toxic, when 20
minutes of midday sunbathing in the summer makes at least 10,000 IU of
vitamin D in our bodies?
In 1999, Reinhold Vieth (pictured right) published a review of vitamin
D research in response to the IOM conclusions. In it, he argued that
there was no evidence that amounts lower than 20,000 IU a day could be
toxic. �Throughout my preparation of this review, I was amazed at the
lack of evidence supporting statements about the toxicity of moderate
doses of vitamin D,� Vieth wrote.
Studies have since shown 10,000 IU a day of vitamin D to be safe.
While any substance will become toxic in excess, vitamin D researchers
today accept that the current vitamin D recommendations could be more
than quadrupled with no fear of toxicity
randall
J,
Does this not bring up the actual cause of psoriasis, crohn's,
rheumatoid arthritis,
and even possibly multiple sclerosis?
Which isn't due to a lack of vitamin D3 or i'd BE CLEAR. RIGHT NOW.
Let's look at what may be the discovery of the century for psoriatics.
Back to the TRUTH about Ai (autoimmune) and gut bugs that screw your
immune system?
OK, what did I post six days ago?
OH?
YOu mean this?
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/b76daa789fa6daa7
or
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/3b4e1e54f340dee8
Sun, Oct 18 2009 11:44 am
Subject: IS THIS the CURE? --> L. Plantarum controls SFB (segmented
filamentous bacteria) & HIGH Levels of Th17
----
Guess WHAT?
This story above for keywords SFB and segmented as keywords is number
1 on the WEB for a google search.
Why is that?
http://www.google.com/search?hl=en&q=sfb+segmented&btnG=Search&aq=f&oq=&aqi=
All I did was look at science and repost it in our little tiny (320
members) psoriasis newsgroup on google:
[use the two above links for ** IS THIS the CURE? L. Plantarum....]
Shall we eat some l. plantarum or do it with the wit kit?
------------
If SFB spurs Th17 in MICE, then you can damn well expect the same
thing in HUMANs.
Or, are you better then a mouse or worm perhaps?
Your genes, many of them identical to a worm or mouse are somehow
different?
Or did all of these folks report this and simply didn't believe it?
From google news in the last week:::
http://www.sciencedaily.com/releases/2009/10/091015123544.htm
In Shaping Our Immune Systems, Some 'Friendly' Bacteria May Play
Inordinate Role
Science Daily (press release) - Oct 15, 2009
ScienceDaily (Oct. 15, 2009) — Out of the trillions of "friendly"
bacteria -- representing hundreds of species -- that make our
intestines their home, ...Gut Bacteria Linked to Immune Response
http://www.medpagetoday.com/Gastroenterology/InflammatoryBowelDisease/16472
MedPage Today - Michael Smith - Oct 16, 2009
Explain to interested patients that this study suggests that -- in
mice at least -- certain ...Friendly Bacteria
http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=22602
Ivanhoe - Oct 15, 2009
(Ivanhoe Newswire) -- New studies offer insight into the constant
dialogue between intestinal microbes and the human immune system,
pointing to a major role ...Unusual bacteria help balance the immune
system in mice
http://www.eurekalert.org/pub_releases/2009-10/nlmc-ubh101409.php
EurekAlert (press release) - Oct 15, 2009
Medical researchers have long suspected that obscure bacteria living
within the intestinal tract may help keep the human immune system in
balance. ...In Shaping Our Immune Systems, Some 'Friendly' Bacteria
May Play Inordinate Role
==============
http://www.medicalnewstoday.com/articles/167690.php
Medical News Today (press release) - Oct 17, 2009
In Shaping Our Immune Systems, Some 'Friendly' Bacteria May Play
Inordinate Role
Out of the trillions of "friendly" bacteria - representing hundreds of
species -that make our intestines their home, new evidence in mice
suggests that it may be a very select few that shape our immune
responses. The findings detailed in two October 16th reports appearing
in the journals Cell and Immunity, both Cell Press publications, offer
new insight into the constant dialogue that goes on between intestinal
microbes and the immune system, and point to a remarkably big role for
a class of microbes known as segmented filamentous bacteria (SFB).
"It's the first example of a commensal bacteria that can induce
accumulation in the gut of a highly specific branch of the immune
system," said Dan Littman of the Howard Hughes Medical Institute and
the New York University School of Medicine, who led the study reported
in Cell. "We're headed into an exciting new area, and we hope more
pieces of how the microbial-host interaction contributes to health
will begin to fall into place."
"Our study provides the surprising result that among the hundreds of
bacterial species composing the gut microbiota -- only a very small
number, the prototype of which is SFB -- can efficiently stimulate the
post-natal physiologic maturation of the immune barrier," added
Valérie Gaboriau-Routhiau of INSERM in France, who led the Immunity
report. "A unique feature of SFB appears to be its capacity to
simultaneously stimulate a large spectrum of intestinal immune
responses -- innate and adaptive, pro-inflammatory and regulatory --
which complete and balance each other."
Notably, those SFBs stimulate particular types of helper T cells,
known as Th17 cells, the studies show.
In Littman's case, the findings by his group were something of an
accidental discovery. They were studying T cells in the intestine and
were getting some inconsistencies in their results. Those
inconsistencies could be traced to differences in the gut floras of
mice obtained from different sources, and specifically, they found, in
the presence or absence of SFB.
Introduction of SFB, but not other bacteria, stimulated the production
of Th17 cells in mice who were otherwise deficient in them, they show.
The bacteria also set in motion a pro-inflammatory gene program. That
SFB-induced immune response protected the mice from becoming ill with
an intestinal pathogen, supporting a role for the SFBs in setting up
the intestine's immunity barrier.
Gaboriau-Routhiau similarly found in studies of conventional and germ-
free mice that colonization of the gut induced a broad spectrum of pro-
inflammatory and T cell responses, including the emergence of Th17
cells. That occurred despite the fact that most bacteria, in
combination or on their own, didn't lead to such a reaction. Rather,
that function appeared limited to a restricted number of bacteria, her
team reports, the prototype of which is the SFB. All on its own, SFB
could largely recapitulate the coordinated maturation of T cell
responses normally induced by the whole mouse microbiota.
Gaboriau-Routhiau suspects that SFBs may have some special attributes
that explain their importance.
"For us, it was first a surprise to observe so little redundancy in
the role of commensal bacteria on stimulating immune responses,"
Gaboriau-Routhiau said. "One striking feature of SFB, which makes it
very different from the vast majority of the members of the
microbiota, is its capacity to adhere to epithelial cells notably in
the ileum, a property normally more the prerogative of pathogens." The
ileum is the final section of the small intestine and is distinguished
by many folds, giving it a very substantial surface area.
The findings also suggest how such commensal bacteria might sometimes
go from beneficial inhabitants, helping to fend off nasty bugs, to
ones that may tip the balance of the immune system toward the
development of inflammatory, autoimmune disease, such as Crohn's
disease, psoriasis and even arthritis, according to the researchers.
Indeed, the Th17 cells observed in the new studies have been noted in
recent years because of their importance in autoimmune diseases,
Littman explained. Animals with defects in those Th17 cells generally
don't develop autoimmune disease or develop disease that is less
severe, earlier studies showed.
"Th17 cells make cytokines that can be highly protective in the case
of infection," he said. "At the same time, in the wrong context or in
the wrong amount [they can lead to disease]. You need to have the
right balance."
Given the bacterial diversity found within our guts, the new results
show how much there still is to learn about this important aspect of
the immune system. While probiotic products on the market today don't
have the benefit of such a thorough understanding, says Littman, there
is little doubt that down the road we may be able to manipulate our
immune system in beneficial ways with microbes. Alternatively, he
said, some of the molecular products of those bacteria - particular
sugars or peptides, for instance - might ultimately serve as useful
therapies on their own.
Cell article:
The researchers include Ivaylo I. Ivanov, New York University School
of Medicine, New York, NY; Koji Atarashi, Osaka University, Osaka,
Japan, Nicolas Manel, New York University School of Medicine, New
York, NY; Eoin L. Brodie, Lawrence Berkeley National Laboratory,
Berkeley, CA, Tatsuichiro Shima, Yakult Central Institute for
Microbiological Research, Kunitachi, Tokyo, Japan, Ulas Karaoz,
Lawrence Berkeley National Laboratory, Berkeley, CA; Dongguang Wei,
Carl Zeiss SMT, Inc., Nanotechnology Systems Division, Peabody, MA;
Katherine C. Goldfarb, Lawrence Berkeley National Laboratory,
Berkeley, CA; Clark A. Santee, Lawrence Berkeley National Laboratory,
Berkeley, CA; Susan V. Lynch, University of California San Francisco,
San Francisco, CA; Takeshi Tanoue, Osaka University, Osaka, Japan;
Akemi Imaoka, Yakult Central Institute for Microbiological Research,
Kunitachi, Tokyo, Japan; Kikuji Itoh, University of Tokyo, Tokyo,
Japan; Kiyoshi Takeda, Osaka University, Osaka, Japan; Yoshinori
Umesaki, Yakult Central Institute for Microbiological Research,
Kunitachi, Tokyo, Japan; Kenya Honda, Osaka University, Osaka, Japan,
Japan Science and Technology Agency, Saitama, Japan; and Dan R.
Littman, New York University School of Medicine, New York, NY, Howard
Hughes Medical Institute.
Immunity article:
The researchers include Vale´ rie Gaboriau-Routhiau, INRA, U910, Unite
´ Ecologie et Physiologie du Syste`me Digestif, Domaine de Vilvert,
Jouy-en-Josas, France, INSERM, Universite´ Paris, Paris, France;
Sabine Rakotobe, INRA, U910, Unite´ Ecologie et Physiologie du
Syste`me Digestif, Domaine de Vilvert, Jouy-en-Josas, France, INSERM,
Universite´ Paris, Paris, France; Emelyne Le´ cuyer, INRA, U910, Unite
´ Ecologie et Physiologie du Syste`me Digestif, Domaine de Vilvert,
Jouy-en-Josas, France, INSERM, Universite´ Paris, Paris, France; Imke
Mulder, University of Aberdeen, Aberdeen, UK; Annai¨g Lan, University
of Aberdeen, Aberdeen, UK; Chantal Bridonneau, INRA, U910, Unite´
Ecologie et Physiologie du Syste`me Digestif, Domaine de Vilvert, Jouy-
en-Josas, France; Violaine Rochet, INRA, U910, Unite´ Ecologie et
Physiologie du Syste`me Digestif, Domaine de Vilvert, Jouy-en-Josas,
France; Annamaria Pisi, University of Bologna, Bologna, Italy;
Marianne De Paepe, INSERM, Universite´ Paris, Paris, France; Giovanni
Brandi, Ge´ rard Eberl, University of Bologna, Bologna, Italy;
Johannes Snel, NIZO Food Research, The Netherlands; Denise Kelly,
University of Aberdeen, Aberdeen, UK; and Nadine Cerf-Bensussan,
INSERM, Universite´ Paris, Paris, France.
Source:
Cathleen Genova
Cell Press
=============
http://www.news-medical.net/news/20091019/Discovery-may-yield-better-understanding-of-protective-gut-dwelling-bacteria.aspx
Discovery may yield better understanding of protective gut-dwelling
bacteria
19. October 2009 06:45
==============
OK, this is boring now.
Till I run the trial and even then you ALL will sit there and say i'm
not gonna
put anything up my yin/yang. LOL
So how about some other things?
Muscle uP you Seniors: YOU CAN DO IT
http://articles.mercola.com/sites/articles/archive/2009/10/24/How-To-Turn-Back-the-Clock-on-Aging-Muscles.aspx
How to Keep Firm Muscle Tone as You Age
by mercola
Scientists have found and manipulated body chemistry linked to the
aging of muscles, and were able to restore the ability of old human
muscle to repair and rebuild itself.
Importantly, the research also found evidence that aging muscles need
to be kept in shape, because long periods of atrophy are more
challenging to overcome. Older muscles do not respond as well to
sudden bouts of exercise. And rather than building muscle, older
people can instead generate scar tissue if they exercise after long
periods of inactivity.
Previous studies have shown that adult muscle stem cells have a
receptor called Notch, which triggers growth when activated. An enzyme
called mitogen-activated protein kinase (MAPK) regulates Notch
activity.
In the lab, the researchers cultured old human muscle and forced the
activation of MAPK. The regenerative ability of the old muscle was
significantly enhanced.
--------------------
[More Mercola]
The H1N1 flu that FLEW the coop?
http://articles.mercola.com/sites/articles/archive/2009/10/24/CBS-Reveals-that-Swine-Flu-Cases-Seriously-Overestimated.aspx
Don't want to read the facts? look at this picture:
http://articles.mercola.com/imageserver/swine-flu.gif
But OTOH Obama says the FLU pandemic is at HAND?
http://www.voanews.com/english/2009-10-24-voa20.cfm
U.S. President Barack Obama has signed a proclamation declaring the
H1N1 swine flu virus a national emergency.
[...]
The World Health Organization says about 5,000 deaths attributed to
H1N1 influenza have been reported worldwide. U.S. health authorities
say more than 1,000 people have died from the virus in the United
States and more than 20,000 people have been hospitalized.
<snip>
Is it the swine flu or simple FLU?
Is he playing loose with the facts or are they counting the numbers of
folks who got the live flu vaccine as H1N1 cases?
And then did suffer a day or two of flu?
So why does mercola say otherwise?
http://articles.mercola.com/sites/articles/archive/2009/10/24/CBS-Reveals-that-Swine-Flu-Cases-Seriously-Overestimated.aspx
Is this stimulus for vaccine producers?
Or a gov panic and NOT a pandemic?
One mans whole family gets h1n1 by david knowles
http://news.aol.com/article/when-h1n1-hits-home-david-knowles/723224
[...]
As I reported Wednesday, a recent study undertaken at Purdue
University estimates that 63 percent of the U.S. population will be
infected with the H1N1 virus. Of that number, 40 percent will become
ill in some way. All in all, 25 percent of all Americans will become
sick as a result of H1N1. The virus should peak between now and the
beginning of November.
<snip>
Then, is obama breaking the rules to save our butts?
http://www.naturalnews.com/027323_swine_flu_national_emergency_pandemic.html
(NaturalNews) According to the CDC, swine flu infections have already
peaked, and the pandemic is on its way out. Peak infection time was
the middle of October, where one in five U.S. children experienced the
flu, says the CDC. Out of nearly 14,000 suspected flu cases tested
during the week ending on October 10, 2009, 99.6% of those were
influenza A, and the vast majority of those were confirmed as H1N1
swine flu infections. (http://www.cdc.gov/flu/weekly/)
Even though the H1N1 pandemic appears to have peaked out, U.S.
President Barack Obama has now declared a national emergency over
swine flu infections. The reasoning behind such a declaration?
According to the White House, it's designed to "allow hospitals to
better handle the surge in patients" by allowing them to bypass
certain federal laws.
<sniP>
http://en.wikipedia.org/wiki/Pandemic
http://en.wikipedia.org/wiki/2009_flu_pandemic
http://en.wikipedia.org/wiki/Emergency_powers
http://en.wikipedia.org/wiki/National_Emergencies_Act
Obama has been playing fast and loose with the
http://en.wikipedia.org/wiki/Constitutional_right
Certainly Walter Williams wasn't OBAMA's Professor when he decided to
spread the wealth around.
A rather socialist, commie thing if ever there was one:
https://www.hillsdale.edu/news/imprimis/archive/issue.asp?year=2009&month=09
Did obama lie to get elected?
You tell me. I didn't vote for him and never will.
And it's not race. I'd vote for Walter Williams any day of the week.
He's a genius. Obama is a puppet of who knows what?
A democrat take over of our gov perhaps?
------------
Time for crap and trade?
Where are those sunspots?
1028 and 1029 are visible RIGHT NOW:
http://sohowww.nascom.nasa.gov/sunspots/
[the site was down today... did obama shut them down? wouldn't
surprise me]
I haven't seen two at once in quite a while.
Global Warming or Global cooling?
Whichever, we are learning more about the giver of life:
http://spie.org/x37587.xml?highlight=x2418&ArticleID=x37587
What some are actually arguing for is less population. With nuclear
energy,
the population is no problem. So how come the evil green morons
don't want to live and LET LIVE with cheap nuclear energy
Because when you exhale CO2, they don't like it and don't
want nuclear anything and they prefer to kill america and suck an egg.
And play with their ego's and sing we are the world as they DIE.
Whoops got on a rant.
But i do feel a tiny bit clearer already?
LOL
randall... SFB is on my radar. Not just gov NUTz....
JRStern
wrote:
>Which isn't due to a lack of vitamin D3 or i'd BE CLEAR. RIGHT NOW.
understood, but I'm interested in the vitamin D even for non-psoriasis
reasons.
>If SFB spurs Th17 in MICE, then you can damn well expect the same
>thing in HUMANs.
Fine. So we want some of these, but not too many. Just how do we
tell how many, and how do we manage the count?
And just because these do affect Th17, it doesn't mean they are the
*only* factor affecting Th17.
And what about our old friend TNF? Are the Th17 the only path to TNF
(I have a vague recollection they are at least *on* the path, or one
of the paths, to TNF)
J.
randall
> On Sat, 24 Oct 2009 19:25:40 -0700 (PDT), randall <ranhu...@aol.com>
> wrote:
>
> >Which isn't due to a lack of vitamin D3 or i'd BE CLEAR. RIGHT NOW.
>
> understood, but I'm interested in the vitamin D even for non-psoriasis
> reasons.
>
> >If SFB spurs Th17 in MICE, then you can damn well expect the same
> >thing in HUMANs.
>
> Fine. So we want some of these, but not too many. Just how do we
> tell how many, and how do we manage the count?
Excuse me. NOT FINE. Why have any excess Th17? Doesn't Th17 hamper
TREG's from turning the immune system OFF after the FACT?
With these VERY SFB's hair like threads:
SEE:
http://www.eurekalert.org/multimedia/pub/17464.php?from=146686
Caption: A little-known bacterial species called segmented
filamentous
bacterium, or SFB, can activate the production of specialized immune
cells in mice. This scanning electron microscope image of an SFB
colony shows a mass of long hair-like filaments created when the
bacteria stay attached to each other after they divide.
If you don't want to believe SFB is in your ileum right now, FINE.
I sorta believe this is our problem. Get rid of SFB and hopefully
immunity will simply go homeostatic again and psoriasis stops.
Till the sFB grows back again should the terrain become hospitable
via diet, alcohol or antibiotics et al.
Certainly ALL of my successful trials point in that direction.
Why else have I concentrated on the GUT since the early 80's?
Simply put, any thing in your diet that disrupts the lacti loving GOOD
FLORA will lead to more plaques.
Been my experience and vice versa.
>
> And just because these do affect Th17, it doesn't mean they are the
> *only* factor affecting Th17.
We shall see if getting rid of these sFB's in the illeum acts as a
cure as
long as their GONE.
Correction. I will.
>
> And what about our old friend TNF?
Without SFB or permeable endotoxin from endogenous bacteria, like SFB,
or simply
called under the umbrella term LPS, the TNF will stop being systemic.
endotoxin
http://en.wikipedia.org/wiki/Lipopolysaccharide
That's the POINT.
http://en.wikipedia.org/wiki/Tumor_necrosis_factor-alpha
Tumor necrosis factor (TNF, cachexin or cachectin and formally known
as tumor necrosis factor-alpha) is a cytokine involved in systemic
inflammation and is a member of a group of cytokines that stimulate
the acute phase reaction.
<snip>
If SFB or some other LPS (endogenous endotoxin Cell Wall) isn't
causing the systemic effect, what is?
PDC's make for IFN. Are they being primed?
http://en.wikipedia.org/wiki/Plasmacytoid_dendritic_cell
Plasmacytoid dendritic cells (pDC) are a rare subtype of circulating
dendritic cells found in the blood as well as in peripheral lymphoid
organs. These cells express the surface markers CD123, BDCA-2(CD303)
and BDCA-4(CD304), but do not express CD11c or CD14, which
distinguishes them from conventional dendritic cells or monocytes,
respectively. As components of the innate immune system, these cells
express intracellular Toll-like receptors 7 and 9, which enable the
detection of viral and bacterial nucleic acids, such as ssRNA or CpG
DNA motifs. Upon stimulation and subsequent activation, these cells
produce large amounts of type I interferon (mainly IFN-α (alpha) and
IFN-β (beta)), which are critical pleiotropic anti-viral compounds
mediating a wide range of effects.
The number of circulating pDCs are found to be declined during chronic
HIV infection as well as HCV infection.
<snip>
http://en.wikipedia.org/wiki/Interferon#Induction_of_interferons
> Are the Th17 the only path to TNF
> (I have a vague recollection they are at least *on* the path, or one
> of the paths, to TNF)
If the above doesn't answer your questions, I can try to make it
clearer.
But perhaps just me becoming clearer will be the conceptual metaphor?
What better analogy? LOL
>
> J.
As to pDC's and IFN...
Let's look...
Ok,
Plasmacytoid dendritic cells and dermatological disorders: focus on
their role in autoimmunity and cancer.
Charles J, Chaperot L, Salameire D, Domizio JD, Aspord C, Gressin R,
Jacob MC, Richard MJ, Beani JC, Plumas J, Leccia MT.
Dendritic cells (DC), considered as immunological sentinels of the
organism since they are antigen presenting cells, create the link
between innate and adaptive immunity. DC include myeloid dendritic
cells (MDC) and plasmacytoid dendritic cells (PDC). The presence of
PDC, cells capable of producing large quantities of _____interferon
alpha (IFN-alpha)____ in response to pathogenic agents or danger
signals, seems to be closely related to pathological conditions. PDC
have been observed in inflammatory immunoallergic dermatological
disorders, in malignant cutaneous tumours and in cutaneous lesions of
infectious origin. They seem to play a crucial role in the initiation
of the pathological processes of autoimmune diseases such as lupus or
psoriasis. Their function within a tumour context is not as well known
and is controversial. They could have a tolerogenic role towards
tumour cells in the absence of an activator but they also have the
capacity to become activated in response to Toll-like receptor (TLR)
ligands and could therefore be useful for therapeutic purposes.
PMID: 19850548
psoria* + interferon 624 hits pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+interferon&log$=activity
Add in TNF as the kicker for 119 hits
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+interferon+TNF&log$=activity
So what pray tell is the pathogenic agent if not SFB?
I've grown tired of saying LPS and permeability.
Though it works for high systemic levels of TNF. But not for IFN?
Am I right?
Oh, i do know that answer. <W>
SFB narrows it down to a REAL HOT ZONE. I've said that over four dozen
times, I bet. LOL
And why wouldn't the appendix (you brought that article to our
attention) be in the same neighbor hood?
WE have the ileum
http://en.wikipedia.org/wiki/Ileum
Appendix and cecum all right there.
So, do you think that SFB made a living there to keep our TNF levels
high and thusly
slow or prevent cancer?
If so, i'd like to avoid the mental aspects next time around. LOL
But look at erin and her minocin. It worked but did it keep working?
We have loads of things that work but then STOP.
When does SFB stop?
Are you actually reading this stuff? LOL
I do KNOW what to DO.
And it will be more then eating some kimchi. <G>
randall....will most Dactylytis also clear? Wow, obama will give me
his peace prize. LOL
zzznot
>> tell how many, and how do we manage the count?
>
>Excuse me. NOT FINE. Why have any excess Th17? Doesn't Th17 hamper
>TREG's from turning the immune system OFF after the FACT?
No.
Warnings for Stelara describe a rare condition in which people have no
Th17, and are very prone to infections.
>Why else have I concentrated on the GUT since the early 80's?
How many guesses do I get?
>If SFB or some other LPS (endogenous endotoxin Cell Wall) isn't
>causing the systemic effect, what is?
It's not systemic, it's in the skin.
>So what pray tell is the pathogenic agent if not SFB?
How many guesses do you need?
>Are you actually reading this stuff? LOL
Mebbe.
J.
randall
I doubt it.
?