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I'm DEAD deaD DEADski! Are you, yet? Cardio & Psoriasis...Heart ATTACK Events -->> Widow Maker -- Vitamin K2 & Parkinson's --C/EBP -alpha Skin Cancer -- St John's WORT Cream- 5HTP day -
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randall
May 12, 2012, 5:02:59 PM5/12/12
to
hi
Hi i'm not trying to make BIG PHARMA rich...
But if you not going to do the vitamin Supplements i TELL you
too....DO..
Then get on statins and do TAKE ENBREL.... Duh..
Or you will BE deadski like ME ski..
Sheessh.
---------------------------
http://medicalxpress.com/news/2012-05-mechanistic-discovery-links-psoriasis-cardiovascular.html
Mechanistic discovery links psoriasis to increased risk of
cardiovascular disease
May 10, 2012 in Diseases, Conditions, Syndromes
The link between psoriasis and cardiovascular events has been observed
for years, however the mechanics were unknown. For the first time,
Case Western Reserve University School of Medicine researchers have
discovered preclinical evidence demonstrating that the inflammatory
skin disease leads to cardiovascular disease. Further, the research
demonstrated that aggressive reversal of psoriasis reduces the
cardiovascular risk as well. Psoriasis is a chronic disease of the
immune system that appears as raised, inflamed, scaly red patches of
skin and is often associated with intense itch. In the United States,
it affects between two and a half to six million patients.
Published in the Journal of Investigative Dermatology, the study used
a new, innovative mouse model to demonstrate a causal connection
between the skin disease and cardiovascular disease. Dr. Ward and her
research team demonstrated that mice engineered to overexpress a
protein called Tie-2 in the skin, develop a skin condition similar to
human psoriasis. Using this model, they showed that persistent,
chronic inflammation confined to the skin can result in inflammation
in large arteries, such as the aorta.
"This discovery is paradigm shifting. There has been a link between
the two diseases but to date we had not been able to show cause.
Epidemiologic evidence from thousands of patients was convincing that
psoriasis patients had a much greater chance of developing
cardiovascular disease and dying from it," says Nicole Ward, PhD,
senior author of the study, assistant professor of dermatology and
neurosciences at Case Western Reserve School of Medicine, and
scientist with the Murdough Family Center for Psoriasis at University
Hospitals Case Medical Center.
There is a known increased risk of heart, cerebrovascular, and
peripheral artery diseases, as well as risk of death, in individuals
suffering from a variety of chronic inflammatory diseases, such as
rheumatoid arthritis (RA), colitis, gum disease, lupus, and psoriasis.
Many researchers showed, statistically, that having psoriasis leads to
an increased risk for cardiovascular disease and heart complications,
however it was unclear why this occurs and it was challenging to
separate out the significance of other lifestyle factors and their
contributions to this risk, she adds.
Based on published clinical reports demonstrating psoriasis patients
had increased risk of developing and dying of heart attack and stroke,
Dr. Ward and her team set-out to investigate whether their mouse model
of psoriasis would also show cardiac complications, mimicking these
seen in human disease. They teamed up with experts in the role of
inflammation in vessel injury – Yunmei Wang, PhD, assistant professor
of medicine at the School of Medicine and Daniel I. Simon, MD the
Herman K. Hellerstein Professor of Cardiovascular Research at the
School of Medicine, and chief, Cardiovascular Medicine at University
Hospitals Case Medical Center.
"We believed that chronic inflammation over a large area of the body
may be the reason for an increased risk of cardiovascular
complications in skin disease patients; however, until now we had no
way to model and definitively prove this," says Dr. Wang.
Dr. Ward and her team measured blood clot formation in the psoriasis
mouse model and normal mice, revealing that time was greatly shortened
in the diseased mice. This shortened time to vessel blockage is akin
to a greater risk for blood vessel blockage in humans that leads to
stroke or heart attack. Further examination revealed that mice with
the skin disease also exhibited inflammation of the vessel wall
similar to that observed with atherosclerotic lesions or plaques.
Importantly, and highly meaningful for patients with psoriasis, Dr.
Ward's work was able to demonstrate that upon reversal of the skin
disease, the cardiovascular inflammation and blood clot formation were
also decreased.
"Our observations of improved vessel wall inflammation and decreased
clot formation following skin-specific repression of disease provide
further evidence that skin inflammation promotes vascular inflammation
and thrombosis and strongly suggests that aggressive treatment of skin
disease may block pathways that produce cardiovascular disease in
psoriasis patients," says Dr. Ward.
Today, Dr. Ward will present these findings at the 2012 Society for
Investigative Dermatology Annual Meeting this week in Raleigh, NC.
<snip>
In for a cardio actual event:
http://en.wikipedia.org/wiki/Tissue_plasminogen_activator
or
http://en.wikipedia.org/wiki/Streptokinase
If you've got the widow maker like Bob Baffert had in Dubai a few
months back
you NEED a STENT.
No tpa or streptokinase is going to be ENOUGH... hence it's called
WIDOW MAKER.
Bob Baffert got very lucky... So he's ALIVE.. i tell YOU... it's ALIVE
and coming to
major RACE TRacks all around the world...
And he WINs THEM
http://en.wikipedia.org/wiki/Bob_Baffert#Personal_life
Wow... look at some of his wins below the personal stuff....WOW..
When he's in Del MAR i'm going to rib him some... as i sit close to
his box.
And he's like our nemesis... as he's SO DARN GOOD at training them
four legged critters.
ok... stupidly segue over... you have to HAVE a HEART... but not two
DRD4 7R alleles...LOL
For that widow maker story from CNN
http://sportsillustrated.cnn.com/2012/writers/tim_layden/04/30/kentucky.derby.bob.baffert/
[....] Here it was the third week in April, 16 days shy of the
Kentucky Derby, and Baffert had finished his morning's work training
(usually) fast and (almost always) expensive horseflesh at his home
base at Santa Anita Park in Arcadia, Calif. The barns, including the
one with a sign that advertises Baffert's three Derby winners, among
other champions, were bathed in sunshine. Stable workers raked the
dirt into neatly harrowed rows. It is a good time to be Baffert the
trainer; in Saturday's 138th Run for the Roses he will saddle
Bodemeister, a horse named after Baffert's seven-year-old son (named
after Baffert's friend, Olympic gold medal-winning skier Bode Miller),
who could be the favorite in the race and, more intriguingly, could
also be an equine monster.
It is a more complicated time to be Baffert the human being, husband
and father. In the early morning hours of March 26 in Dubai, United
Arab Emirates, Baffert, 59, suffering from nausea, chest pains,
soreness in his left arm and pretty much every other symptom listed in
Wikipedia under ''heart attack,'' underwent an emergency procedure in
which stents were inserted in two major coronary arteries. One of
them, the proximal left anterior descending coronary artery (aka "The
Widow maker''), was 100 percent blocked; another was 90 percent
blocked. After the procedure Baffert's surgeon told him: "You were
lucky, maybe moments away from going into cardiac arrest.''
That part is not intended to be funny. Nor is this: "I really do feel
lucky,'' said Baffert, sitting on his office couch, sans his trademark
sunglasses. "I'm getting a second chance. A lot of things could have
happened differently and I'd be dead.''
<snip>
Read more: Baffert:
http://sportsillustrated.cnn.com/2012/writers/tim_layden/04/30/kentucky.derby.bob.baffert/index.html
He did come within a nose or so at the Kentucky Derby this year with A
horse named after his Son , Body.
If that isn't enough to give ONE a heart attack... yak yak... i don't
know what is...
Back to the top story... cardio wise..
The only abstract i find for (author) Ward is from 2009 but it came
out recently?
huh?
I posted it before in 2009.
So it had to come out earlier? I'm confused.
Let's see it again.
PMID: 19342373
And look at ALL of dr. Ward's abstracts:
52 hits - Ward NL[Author] - pubmed-
http://www.ncbi.nlm.nih.gov/pubmed?term=Ward%20NL%5BAuthor%5D&cauthor=true&cauthor_uid=19342373
NINE of ward's 52 are : psoria*
http://www.ncbi.nlm.nih.gov/pubmed?term=Ward%20NL%5BAuthor%5D%20psoria*
OK and PMID: 19342373 is # 8 of 9 , so Ward's second psoriasis study
out of nine:
And #1 of 9 goes with the top article i SEE NOW or it JUST NOW poPPed
up on pubmed:
<randall note or due to it being stuck to the author search? LOL ...
duh i'm stuPidly now / again... LOL>>>
http://www.ncbi.nlm.nih.gov/pubmed/22572815
J Invest Dermatol. 2012 May 10. doi: 10.1038/jid.2012.112.
Chronic Skin-Specific Inflammation Promotes Vascular Inflammation and
Thrombosis.
Wang Y, Gao H, Loyd CM, Fu W, Diaconu D, Liu S, Cooper KD, McCormick
TS, Simon DI, Ward NL.
Source
1] Department of Medicine, Division of Cardiovascular Medicine, Case
Western Reserve University, Cleveland, Ohio, USA [2] The Harrington
Heart and Vascular Institute, University Hospitals Case Medical
Center, Cleveland, Ohio, USA.
Abstract
Patients with psoriasis have systemic and vascular inflammation and
are at increased risk for myocardial infarction, stroke, and
cardiovascular death. However, the underlying mechanism(s) mediating
the link between psoriasis and vascular disease is incompletely
defined. This study sought to determine whether chronic skin-specific
inflammation has the capacity to promote vascular inflammation and
thrombosis. Using the KC-Tie2 doxycycline-repressible (Dox-off) murine
model of psoriasiform skin disease, spontaneous aortic root
inflammation was observed in 33% of KC-Tie2 compared with 0% of
control mice by 12 months of age (P=0.04) and was characterized by the
accumulation of macrophages, T lymphocytes, and B lymphocytes, as well
as by reduced collagen content and increased elastin breaks.
Importantly, aortic inflammation was preceded by increases in serum
tumor necrosis factor-α, IL-17A, vascular endothelial growth factor,
IL-12, monocyte chemotactic protein-1, and S100A8/A9, as well as
splenic and circulating CD11b(+)Ly-6C(hi) pro-inflammatory monocytes.
Doxycycline treatment of old mice with severe skin disease eliminated
skin inflammation and the presence of aortic root lesion in 1-year-old
KC-Tie2 animals. Given the bidirectional link between inflammation and
thrombosis, arterial thrombosis was assessed in KC-Tie2 and control
mice; mean time to occlusive thrombus formation was shortened by 64%
(P=0.002) in KC-Tie2 animals; and doxycycline treatment returned
thrombosis clotting times to that of control mice (P=0.69). These
findings demonstrate that sustained skin-specific inflammation
promotes aortic root inflammation and thrombosis and suggest that
aggressive treatment of skin inflammation may attenuate pro-
inflammatory and pro-thrombotic pathways that produce cardiovascular
disease in psoriasis patients.Journal of Investigative Dermatology
advance online publication, 10 May 2012; doi:10.1038/jid.2012.112.
PMID: 22572815
And going back to...
Tie it to tie2 and don't DIE (cardio event like the widow maker?)
while doing it please?
OK... stop the infernal pressure... your killing me... already... LoL
http://www.ncbi.nlm.nih.gov/pubmed/19342373
Am J Pathol. 2009 Apr;174(4):1443-58.
Keratinocyte but not endothelial cell-specific overexpression of Tie2
leads to the development of psoriasis.
Wolfram JA, Diaconu D, Hatala DA, Rastegar J, Knutsen DA, Lowther A,
Askew D, Gilliam AC, McCormick TS, Ward NL.
Source
Case Western Reserve University, Department of Dermatology, 10900
Euclid Ave, Cleveland, OH 44106, USA.
Abstract
Psoriasis is initiated and maintained through a multifaceted interplay
between keratinocytes, blood vessels, gene expression, and the immune
system. One previous psoriasis model demonstrated that overexpression
of the angiopoietin receptor Tie2 in endothelial cells and
keratinocytes led to the development of a psoriasiform phenotype;
however, the etiological significance of overexpression in each cell
type alone was unclear. We have now engineered two new mouse models
whereby Tie2 expression is confined to either endothelial cells or
keratinocytes. Both lines of mice have significant increases in dermal
vasculature but only the KC-Tie2-overexpressing mice developed a
cutaneous psoriasiform phenotype. These mice spontaneously developed
characteristic hallmarks of human psoriasis, including extensive
acanthosis, increases in dermal CD4(+) T cells, infiltrating epidermal
CD8(+) T cells, dermal dendritic cells and macrophages, and increased
expression of cytokines and chemokines associated with psoriasis,
including interferon-gamma, tumor necrosis factor-alpha, and
interleukins 1alpha, 6, 12, 22, 23, and 17. Host-defense molecules,
cathelicidin, beta-defensin, and S100A8/A9, were also up-regulated in
the hyperproliferative skin. All of the phenotypic traits were
completely reversed without any scarring following repression of the
transgene and were significantly improved following treatment with the
anti-psoriasis systemic therapeutic, cyclosporin A. Therefore,
confining Tie2 overexpression solely to keratinocytes results in a
mouse model that meets the clinical, histological, immunophenotypic,
biochemical, and pharmacological criteria required for an animal model
of human psoriasis.
PMID: 19342373
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19342373/?tool=pubmed
OK so let's see it from 2009 in the P NG?
OK
one hit -
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=PMID%3A+19342373+&start=0&
to
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/d4c7bb61be46d9e/343a42bc8a920114?hl=en&lnk=gst&q=tie2#343a42bc8a920114
And several-- tie2 hits:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=tie2&start=0&hl=en&
And the first tie hit is this pmid: (but we didn't have the pmid # but
did have the abstract)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/d4c7bb61be46d9e/343a42bc8a920114?hl=en&lnk=gst&q=tie2#343a42bc8a920114
OK so PMID: 19342373 made a big stir and the pmid # came out a day or
two later:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/3e764f9d50e3d1d7
And now we've tied PMID: 22572815 to PMID: 19342373 from 2009.
Nice.... so i can stop having my widow maker and make some wise
observations, already...LOL
And ward's #2 of 52 is tie2 in a mouse model with botulinum.
let's see:
http://www.ncbi.nlm.nih.gov/pubmed/22418873
J Invest Dermatol. 2012 Mar 15. doi: 10.1038/jid.2012.60.
Botulinum Neurotoxin A Decreases Infiltrating Cutaneous Lymphocytes
and Improves Acanthosis in the KC-Tie2 Mouse Model.
Ward NL, Kavlick KD, Diaconu D, Dawes SM, Michaels KA, Gilbert E.
Source
1] Department of Dermatology, Case Western Reserve University,
Cleveland, Ohio, USA [2] Department of Neurosciences, Case Western
Reserve University, Cleveland, Ohio, USA [3] The Murdough Family
Center for Psoriasis, University Hospitals Case Medical Center,
Cleveland, Ohio, USA.
PMID: 22418873
This one from this year has psor meat in it... or i'll find it..
http://www.ncbi.nlm.nih.gov/pubmed/22295141
Int J Clin Exp Pathol. 2012;5(1):1-11. Epub 2012 Jan 1.
Transgenic overexpression of keratinocyte-specific VEGF and Ang1 in
combination promotes wound healing under nondiabetic but not diabetic
conditions.
Loyd CM, Diaconu D, Fu W, Adams GN, Brandt E, Knutsen DA, Wolfram JA,
McCormick TS, Ward NL.
Source
Department of Dermatology, Case Western Reserve University Cleveland,
OH 44106, USA.
Abstract
VEGF and Angiopoietin (Ang)1 are growth factors that independently
improve wound healing outcomes. Using a tet-repressible mouse model
coupled with streptozotocin-induced diabetes, we examined wound
healing in diabetic and nondiabetic mice engineered to overexpress
keratinocyte-specific (K5) VEGF, Ang1 or Ang1-VEGF combined. All
nondiabetic mice healed more rapidly than their diabetic counterparts;
however overexpression of VEGF, Ang1 or the combination failed to
improve wound closure under diabetic conditions. Conversely, under
nondiabetic conditions, combining Ang1 and VEGF resulted in rapid
wound closure. Molecular analyses of diabetic and nondiabetic K5-Ang1-
VEGF skin revealed no differences in VEGF expression but an 80%
decrease in Ang1 under diabetic conditions, suggesting an integral
role for Ang1. Nondiabetic K5-Ang1 mice healed more quickly and had
significant increases in granulation tissue and a 60% decrease in re-
epithelialization 7 days after wounding. Furthermore, Ang1 stimulated
primary mouse keratinocytes showed significantly less migration into a
wound bed in an in vitro wound healing bioassay and had decreased
pMAPK, pNFκB, pAkt, and pStat3 signaling. These data suggest that
combined Ang1-VEGF overexpression cannot overcome diabetes-induced
delays in wound healing but is efficacious under nondiabetic
conditions possibly via Ang1-mediated delays in re-epithelialization
and enhancement of granulation tissue formation, thereby allowing more
rapid secondary intention healing.
PMID: 22295141
Free PMC Article
176 hits for: psoria* + vegf -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20vegf
2 of 176 also have ANG1
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20vegf%20ang1
But the first one shows ANG2
And we still get : 2 hits: ang2 + psoria* + vegf -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20vegf%20ang2
==============
http://medicalxpress.com/news/2012-05-vitamin-k2-parkinson-patients.html
Vitamin K2: New hope for Parkinson's patients?
May 11, 2012 in Parkinson's & Movement disorders
Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven,
succeeded in undoing the effect of one of the genetic defects that
leads to Parkinson's using vitamin K2. His discovery gives hope to
Parkinson's patients. This research was done in collaboration with
colleagues from Northern Illinois University (US) and will be
published this evening on the website of the authorative journal
Science.
"It appears from our research that administering vitamin K2 could
possibly help patients with Parkinson's. However, more work needs to
be done to understand this better," says Patrik Verstreken.
Malfunctioning power plants are at the basis of Parkinson's.
If we looked at cells as small factories, then mitochondria would be
the power plants responsible for supplying the energy for their
operation. They generate this energy by transporting electrons. In
Parkinson's patients, the activity of mitochondria and the transport
of electrons have been disrupted, resulting in the mitochondria no
longer producing sufficient energy for the cell. This has major
consequences as the cells in certain parts of the brain will start
dying off, disrupting communication between neurons. The results are
the typical symptoms of Parkinson's: lack of movement (akinesia),
tremors and muscle stiffness.
The exact cause of this neurodegenerative disease is not known. In
recent years, however, scientists have been able to describe several
genetic defects (mutations) found in Parkinson's patients, including
the so-called PINK1 and Parkin mutations, which both lead to reduced
mitochondrial activity. By studying these mutations, scientists hope
to unravel the mechanisms underlying the disease process.
Paralyzed fruit flies
Fruit flies (Drosophila) are frequently used in lab experiments
because of their short life spans and breeding cycles, among other
things. Within two weeks of her emergence, every female is able to
produce hundreds of offspring. By genetically modifying fruitflies,
scientists can study the function of certain genes and proteins.
Patrik Verstreken and his team used fruitflies with a genetic defect
in PINK1 or Parkin that is similar to the one associated with
Parkinson's. They found that the flies with a PINK1 or Parkin mutation
lost their ability to fly.
Upon closer examination, they discovered that the mitochondria in
these flies were defective, just as in Parkinson's patients. Because
of this they generated less intracellular energy – energy the insects
needed to fly. When the flies were given vitamin K2, the energy
production in their mitochondria was restored and the insects' ability
to fly improved. The researchers were also able to determine that the
energy production was restored because the vitamin K2 had improved
electron transport in the mitochondria. This in turn led to improved
energy production.
Conclusion
Vitamin K2 plays a role in the energy production of defective
mitochondria. Because defective mitochondria are also found in
Parkinson's patients with a PINK1 or Parkin mutation, vitamin K2
potentially offers hope for a new treatment for Parkinson's.
<snip>
LOOK go buy some Miso and EAT it... or greens... full of k2... it's
GOOD for YOU..
and might stop that heart attack... i eat the miso with a spoon when
i'm to lazy to put it in hot O2.
======================
C/EBP alpha needed to prevent skin cancer:
http://en.wikipedia.org/wiki/CEBPA
Symbols CEBPA; C/EBP-alpha; CEBP
CCAAT/enhancer-binding protein alpha is a protein that in humans is
encoded by the CEBPA gene.[1][2] The protein encoded by this
intronless gene is a bZIP transcription factor which can bind as a
homodimer to certain promoters and enhancers. It can also form
heterodimers with the related proteins CEBP-beta and CEBP-gamma. The
encoded protein has been shown to bind to the promoter and modulate
the expression of the gene encoding leptin, a protein that plays an
important role in body weight homeostasis. Also, the encoded protein
can interact with CDK2 and CDK4, thereby inhibiting these kinases and
causing growth arrest in cultured cells.[3]
Interactions
CEBPA has been shown to interact with Cyclin-dependent kinase 2[4] and
Cyclin-dependent kinase 4.[4]
<snip>
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/dcdd406a7091e423/2565c88a3d2b6e66?lnk=gst&q=CEBPa#2565c88a3d2b6e66
[...] http://www.medicalnewstoday.com/articles/185087.php
The Rewiring Of Gene Regulation Across 300 Million Years Of Evolution
As published in Science, researchers from Cambridge, Glasgow and
Greece have discovered a remarkable amount of plasticity in how
transcription factors, the proteins that bind to DNA to control the
activation of genes, maintain their function over large evolutionary
distances.
The text books tell us that transcription factors recognise the genes
that they regulate by binding to short, sequence-specific lengths of
DNA upstream or downstream of their target genes. It was widely
assumed that, like the sequences of the genes themselves, these
transcription factor binding sites would be highly conserved
throughout evolution. However, this turns out not to be the case in
mammals.
The authors traced the evolution of gene regulation by comparing the
binding of evolutionarily conserved transcription factors in the
genomes of five vertebrate species - human, dog, mouse, short-tailed
opossum and chicken - spanning 300 million years.
In all tested species, the transcription factors CEBPA and HNF4A are
master regulators of liver-specific genes. By mapping the binding of
CEBPA and HNF4A in the genomes of each species and comparing those
maps, they found that in most cases neither the site nor the sequence
of the transcription factor binding sites is conserved, yet despite
this, these transcription factors still manage to regulate the
largely
conserved gene expression and function of liver tissue.
<sniP>
Is there any latest news on it?
checking:
http://medicalxpress.com/latest-news/
NOPE : this is old news:
http://medicalxpress.com/news/2011-05-lack-gatekeeper-protein-linked-skin.html
Lack of 'gatekeeper' protein linked to skin cancer
May 18, 2011 in Cancer
New research from North Carolina State University shows that a
"gatekeeper" protein plays an important role in skin-cancer prevention
in humans and lab mice.
The protein, C/EBP alpha, is normally abundantly expressed to help
protect skin cells from DNA damage when humans are exposed to
sunlight. The NC State research shows, however, that the protein is
not expressed when certain human skin cancers are present.
Moreover, when the protein is inactivated in special lab mice exposed
to small amounts of the UVB solar radiation, the mice become more
susceptible to skin cancer.
Dr. Robert Smart, professor of environmental and molecular toxicology
at NC State and the corresponding author of a paper in the Journal of
Investigative Dermatology describing the research, says that C/EBP
alpha serves as an important "pause button" in cells. If there is any
DNA damage, C/EBP alpha halts the cell-replication process to allow
time for cells to repair themselves to prevent DNA errors from
occurring.
"Loss of C/EBP alpha expression is associated with some of the most
common human cancers, including breast and colon cancer," Smart says.
"We think it may also have a role in tumor suppression in these
cancers via its gatekeeper function."
In the study, the researchers found that human skin expresses C/EBP
alpha as does the pre-cancerous, benign lesion called actinic keratose
– the precursor to skin cancer.
"C/EBP alpha is expressed in normal human skin and in pre-cancerous
actinic keratoses, but something happens when cancerous lesions appear
– the protein is not expressed," Smart says. "We then asked, 'Is the
loss of C/EBP alpha contributing to tumor formation?' The answer seems
to be yes."
Smart and colleagues exposed hairless, genetically modified mice –
bred with C/EBP alpha inactivated – to low doses of the UVB solar
radiation. The mice were highly susceptible to certain common types of
skin cancer – squamous cell carcinomas – with these cancerous tumors
developing and growing rapidly.
"If you can figure out how to keep C/EBP alpha turned on, maybe the
tumor would stay in its pre-cancerous state," Smart says.
Smart adds that figuring out how the protein fulfills its gatekeeper
role – and how and why the protein is inactivated in cancerous cells –
marks the next step in his research.
More information: "C/EBP alpha Expression is Downregulated in Human
Nonmelanoma Skin Cancers and Inactivation of C/EBP alpha Confers
Susceptibility to UVB-Induced Skin Squamous Cell Carcinomas" Elizabeth
A. Thompson, et al. Published: June 2011 print edition of Journal of
Investigative Dermatology
Abstract
Human epidermis is routinely subjected to DNA damage induced by UVB
solar radiation. Cell culture studies have revealed an unexpected role
for C/EBP alpha (CCAAT/enhancer-binding protein-alpha) in the DNA
damage response network, where C/EBP alpha is induced following UVB
DNA damage, regulates the G1 checkpoint, and diminished or ablated
expression of C/EBP alpha results in G1 checkpoint failure. In the
current study we observed that C/EBP alpha is induced in normal human
epidermal keratinocytes and in the epidermis of human subjects exposed
to UVB radiation. The analysis of human skin precancerous and
cancerous lesions (47 cases) for C/EBP alpha expression was conducted.
Actinic keratoses, a precancerous benign skin growth and precursor to
squamous cell carcinoma (SCC), expressed levels of C/EBP alpha similar
to normal epidermis. Strikingly, all invasive SCCs no longer expressed
detectable levels of C/EBP alpha. To determine the significance of C/
EBP alpha in UVB-induced skin cancer, SKH-1 mice lacking epidermal C/
EBP alpha (CKO alpha) were exposed to UVB. CKO alpha mice were highly
susceptible to UVB-induced SCCs and exhibited accelerated tumor
progression. CKO alpha mice displayed keratinocyte cell cycle
checkpoint failure in vivo in response to UVB that was characterized
by abnormal entry of keratinocytes into S phase. Our results
demonstrate that C/EBP alpha is silenced in human SCC and loss of C/
EBP alpha confers susceptibility to UVB-induced skin SCCs involving
defective cell cycle arrest in response to UVB.
===============
St john's wort:
http://www.ncbi.nlm.nih.gov/pubmed/22571563
Australas J Dermatol. 2012 May;53(2):131-5. doi: 10.1111/j.
1440-0960.2012.00877.x. Epub 2012 Mar 8.
The evaluation of the clinical effect of topical St Johns wort
(Hypericum perforatum L.) in plaque type psoriasis vulgaris: A pilot
study.
Najafizadeh P, Hashemian F, Mansouri P, Farshi S, Surmaghi MS,
Chalangari R.
Source
Department of Pharmacology, Pharmaceutical Sciences Branch, Islamic
Azad University Department of Clinical Pharmacy, Pharmaceutical
Sciences Branch, Islamic Azad University Department of Dermatology,
Imam Hospital, Tehran University of Medical Sciences Skin and Stem
Cell Research Center Department of Pharmacognosy, Faculty of Pharmacy,
Tehran University of Medical Sciences, Tehran, Iran.
Abstract
In this case series, ten patients with plaque-type psoriasis were
treated with Hypericum perforatum ointment. The hypericum ointment was
applied to one side of each patient's body and the vehicle to the
opposite side twice daily for 4 weeks in a single blinded manner.
Modified psoriasis area severity index (PASI) scores were
significantly lowered where the formulated ointment had been applied.
In determining PASI scores, three factors, erythema, scaling and
thickness, were evaluated; all were significantly lower where the
formulated ointment had been applied (P = 0.01, P = 0.004, P = 0.04).
Hypericum perforatum ointment applied twice daily may be effective in
reducing PASI scores in mild plaque-type psoriasis, however, further
larger studies need be conducted to achieve a more conclusive result.
PMID: 22571563
115 hits: john's wort - p ng
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=+john%27s+wort&start=0&hl=en&
17 hits: Hypericum
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=Hypericum+&start=0&hl=en&
Hypericum perforatum - 9 hits - p ng:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=Hypericum+perforatum+&start=0&hl=en&
And i've got some good info in this THREAD:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/c51c599ee125d14a/76469b4a2421d541?hl=en&lnk=gst&q=Hypericum+perforatum+#76469b4a2421d541
OK i've got to GO WATCH my Nephews BASEBALL game...s
I hope i don't have ONE of these cardio BAD days... not like bad hair
days..LOL.... taking some fish oils..... next... LOL
http://en.wikipedia.org/wiki/Widow_maker
A widow maker is a nickname used to describe a highly stenotic left
main coronary artery or proximal left anterior descending coronary
artery of the heart.
This term is used because if the artery gets abruptly and completely
occluded it will cause a massive heart attack that will likely lead to
a sudden death. The blockage that kills is made up of platelets
streaming to the site of a ruptured cholesterol plaque. Even a small
amount of plaque in this area can (for a variety of poorly understood
reasons) rupture and cause death; bypassing chronic blockages or
trying to open them up with angioplasty does not prevent heart attack
but it can restore blood flow in case of a sudden blockage or heart
attack. An example of the devastating results of a complete occlusion
of the LAD (Left Anterior Descending) artery was the sudden death of
former NBC News Washington Bureau Chief Tim Russert.
From the minute a widow maker hits, survival time ranges from minutes
to several hours. Rapidly progressing symptoms should signal need for
immediate attention. Symptoms of initial onset may include nausea,
shortness of breath, pain in the head, jaw, arms or chest, often of a
novel but imprecise sensation which builds with irregular heart beat.
Early symptoms may be mistaken for food poisoning, flu or general
malaise until they intensify. A widow maker cannot kill
instantaneously but induce cardiac arrest which may do so within 10 to
20 minutes of no circulation. A victim with no pulse or breath is
still alive living off oxygen stored in the blood and may be able to
be rescued if treatment is begun promptly within this window. [1].
<snip>
Did Russert have some fish oil in his diet?
What's that other stuff i say to take... i took ONE and i'm in the
PINK today..
Oh yeah... 5HTP from africa.. the little black
http://en.wikipedia.org/wiki/Griffonia_simplicifolia
Griffonia simplicifolia (syn. Bandeiraea simplicifolia Benth.) is a
woody climbing shrub native to West Africa and Central Africa. It
grows to about 3 m, and bears greenish flowers followed by black pods.
Chemical constituents
The seeds of the plant are used as an herbal supplement for their 5-
hydroxytryptophan (5-HTP ) content.[2][3] 5-Hydroxytryptophan is an
important building block for the human body to form serotonin.[4]
Serotonin plays an important role in the body specially as a
neurotransmitter to transport signals between neurons in the nervous
system. Griffonia simplicifolia also has a legume lectin called GS
Isolectin B4, which binds to alpha-D-galactosyl residues of
polysaccharides and glycoproteins.
<snip.>
I'm gonna take two of these dudes... i'm feeling xlnt.
randall... living large and getting UVB's from the sun = D3 in ME...
Hi i'm not trying to make BIG PHARMA rich...
But if you not going to do the vitamin Supplements i TELL you
too....DO..
Then get on statins and do TAKE ENBREL.... Duh..
Or you will BE deadski like ME ski..
Sheessh.
---------------------------
http://medicalxpress.com/news/2012-05-mechanistic-discovery-links-psoriasis-cardiovascular.html
Mechanistic discovery links psoriasis to increased risk of
cardiovascular disease
May 10, 2012 in Diseases, Conditions, Syndromes
The link between psoriasis and cardiovascular events has been observed
for years, however the mechanics were unknown. For the first time,
Case Western Reserve University School of Medicine researchers have
discovered preclinical evidence demonstrating that the inflammatory
skin disease leads to cardiovascular disease. Further, the research
demonstrated that aggressive reversal of psoriasis reduces the
cardiovascular risk as well. Psoriasis is a chronic disease of the
immune system that appears as raised, inflamed, scaly red patches of
skin and is often associated with intense itch. In the United States,
it affects between two and a half to six million patients.
Published in the Journal of Investigative Dermatology, the study used
a new, innovative mouse model to demonstrate a causal connection
between the skin disease and cardiovascular disease. Dr. Ward and her
research team demonstrated that mice engineered to overexpress a
protein called Tie-2 in the skin, develop a skin condition similar to
human psoriasis. Using this model, they showed that persistent,
chronic inflammation confined to the skin can result in inflammation
in large arteries, such as the aorta.
"This discovery is paradigm shifting. There has been a link between
the two diseases but to date we had not been able to show cause.
Epidemiologic evidence from thousands of patients was convincing that
psoriasis patients had a much greater chance of developing
cardiovascular disease and dying from it," says Nicole Ward, PhD,
senior author of the study, assistant professor of dermatology and
neurosciences at Case Western Reserve School of Medicine, and
scientist with the Murdough Family Center for Psoriasis at University
Hospitals Case Medical Center.
There is a known increased risk of heart, cerebrovascular, and
peripheral artery diseases, as well as risk of death, in individuals
suffering from a variety of chronic inflammatory diseases, such as
rheumatoid arthritis (RA), colitis, gum disease, lupus, and psoriasis.
Many researchers showed, statistically, that having psoriasis leads to
an increased risk for cardiovascular disease and heart complications,
however it was unclear why this occurs and it was challenging to
separate out the significance of other lifestyle factors and their
contributions to this risk, she adds.
Based on published clinical reports demonstrating psoriasis patients
had increased risk of developing and dying of heart attack and stroke,
Dr. Ward and her team set-out to investigate whether their mouse model
of psoriasis would also show cardiac complications, mimicking these
seen in human disease. They teamed up with experts in the role of
inflammation in vessel injury – Yunmei Wang, PhD, assistant professor
of medicine at the School of Medicine and Daniel I. Simon, MD the
Herman K. Hellerstein Professor of Cardiovascular Research at the
School of Medicine, and chief, Cardiovascular Medicine at University
Hospitals Case Medical Center.
"We believed that chronic inflammation over a large area of the body
may be the reason for an increased risk of cardiovascular
complications in skin disease patients; however, until now we had no
way to model and definitively prove this," says Dr. Wang.
Dr. Ward and her team measured blood clot formation in the psoriasis
mouse model and normal mice, revealing that time was greatly shortened
in the diseased mice. This shortened time to vessel blockage is akin
to a greater risk for blood vessel blockage in humans that leads to
stroke or heart attack. Further examination revealed that mice with
the skin disease also exhibited inflammation of the vessel wall
similar to that observed with atherosclerotic lesions or plaques.
Importantly, and highly meaningful for patients with psoriasis, Dr.
Ward's work was able to demonstrate that upon reversal of the skin
disease, the cardiovascular inflammation and blood clot formation were
also decreased.
"Our observations of improved vessel wall inflammation and decreased
clot formation following skin-specific repression of disease provide
further evidence that skin inflammation promotes vascular inflammation
and thrombosis and strongly suggests that aggressive treatment of skin
disease may block pathways that produce cardiovascular disease in
psoriasis patients," says Dr. Ward.
Today, Dr. Ward will present these findings at the 2012 Society for
Investigative Dermatology Annual Meeting this week in Raleigh, NC.
<snip>
In for a cardio actual event:
http://en.wikipedia.org/wiki/Tissue_plasminogen_activator
or
http://en.wikipedia.org/wiki/Streptokinase
If you've got the widow maker like Bob Baffert had in Dubai a few
months back
you NEED a STENT.
No tpa or streptokinase is going to be ENOUGH... hence it's called
WIDOW MAKER.
Bob Baffert got very lucky... So he's ALIVE.. i tell YOU... it's ALIVE
and coming to
major RACE TRacks all around the world...
And he WINs THEM
http://en.wikipedia.org/wiki/Bob_Baffert#Personal_life
Wow... look at some of his wins below the personal stuff....WOW..
When he's in Del MAR i'm going to rib him some... as i sit close to
his box.
And he's like our nemesis... as he's SO DARN GOOD at training them
four legged critters.
ok... stupidly segue over... you have to HAVE a HEART... but not two
DRD4 7R alleles...LOL
For that widow maker story from CNN
http://sportsillustrated.cnn.com/2012/writers/tim_layden/04/30/kentucky.derby.bob.baffert/
[....] Here it was the third week in April, 16 days shy of the
Kentucky Derby, and Baffert had finished his morning's work training
(usually) fast and (almost always) expensive horseflesh at his home
base at Santa Anita Park in Arcadia, Calif. The barns, including the
one with a sign that advertises Baffert's three Derby winners, among
other champions, were bathed in sunshine. Stable workers raked the
dirt into neatly harrowed rows. It is a good time to be Baffert the
trainer; in Saturday's 138th Run for the Roses he will saddle
Bodemeister, a horse named after Baffert's seven-year-old son (named
after Baffert's friend, Olympic gold medal-winning skier Bode Miller),
who could be the favorite in the race and, more intriguingly, could
also be an equine monster.
It is a more complicated time to be Baffert the human being, husband
and father. In the early morning hours of March 26 in Dubai, United
Arab Emirates, Baffert, 59, suffering from nausea, chest pains,
soreness in his left arm and pretty much every other symptom listed in
Wikipedia under ''heart attack,'' underwent an emergency procedure in
which stents were inserted in two major coronary arteries. One of
them, the proximal left anterior descending coronary artery (aka "The
Widow maker''), was 100 percent blocked; another was 90 percent
blocked. After the procedure Baffert's surgeon told him: "You were
lucky, maybe moments away from going into cardiac arrest.''
That part is not intended to be funny. Nor is this: "I really do feel
lucky,'' said Baffert, sitting on his office couch, sans his trademark
sunglasses. "I'm getting a second chance. A lot of things could have
happened differently and I'd be dead.''
<snip>
Read more: Baffert:
http://sportsillustrated.cnn.com/2012/writers/tim_layden/04/30/kentucky.derby.bob.baffert/index.html
He did come within a nose or so at the Kentucky Derby this year with A
horse named after his Son , Body.
If that isn't enough to give ONE a heart attack... yak yak... i don't
know what is...
Back to the top story... cardio wise..
The only abstract i find for (author) Ward is from 2009 but it came
out recently?
huh?
I posted it before in 2009.
So it had to come out earlier? I'm confused.
Let's see it again.
PMID: 19342373
And look at ALL of dr. Ward's abstracts:
52 hits - Ward NL[Author] - pubmed-
http://www.ncbi.nlm.nih.gov/pubmed?term=Ward%20NL%5BAuthor%5D&cauthor=true&cauthor_uid=19342373
NINE of ward's 52 are : psoria*
http://www.ncbi.nlm.nih.gov/pubmed?term=Ward%20NL%5BAuthor%5D%20psoria*
OK and PMID: 19342373 is # 8 of 9 , so Ward's second psoriasis study
out of nine:
And #1 of 9 goes with the top article i SEE NOW or it JUST NOW poPPed
up on pubmed:
<randall note or due to it being stuck to the author search? LOL ...
duh i'm stuPidly now / again... LOL>>>
http://www.ncbi.nlm.nih.gov/pubmed/22572815
J Invest Dermatol. 2012 May 10. doi: 10.1038/jid.2012.112.
Chronic Skin-Specific Inflammation Promotes Vascular Inflammation and
Thrombosis.
Wang Y, Gao H, Loyd CM, Fu W, Diaconu D, Liu S, Cooper KD, McCormick
TS, Simon DI, Ward NL.
Source
1] Department of Medicine, Division of Cardiovascular Medicine, Case
Western Reserve University, Cleveland, Ohio, USA [2] The Harrington
Heart and Vascular Institute, University Hospitals Case Medical
Center, Cleveland, Ohio, USA.
Abstract
Patients with psoriasis have systemic and vascular inflammation and
are at increased risk for myocardial infarction, stroke, and
cardiovascular death. However, the underlying mechanism(s) mediating
the link between psoriasis and vascular disease is incompletely
defined. This study sought to determine whether chronic skin-specific
inflammation has the capacity to promote vascular inflammation and
thrombosis. Using the KC-Tie2 doxycycline-repressible (Dox-off) murine
model of psoriasiform skin disease, spontaneous aortic root
inflammation was observed in 33% of KC-Tie2 compared with 0% of
control mice by 12 months of age (P=0.04) and was characterized by the
accumulation of macrophages, T lymphocytes, and B lymphocytes, as well
as by reduced collagen content and increased elastin breaks.
Importantly, aortic inflammation was preceded by increases in serum
tumor necrosis factor-α, IL-17A, vascular endothelial growth factor,
IL-12, monocyte chemotactic protein-1, and S100A8/A9, as well as
splenic and circulating CD11b(+)Ly-6C(hi) pro-inflammatory monocytes.
Doxycycline treatment of old mice with severe skin disease eliminated
skin inflammation and the presence of aortic root lesion in 1-year-old
KC-Tie2 animals. Given the bidirectional link between inflammation and
thrombosis, arterial thrombosis was assessed in KC-Tie2 and control
mice; mean time to occlusive thrombus formation was shortened by 64%
(P=0.002) in KC-Tie2 animals; and doxycycline treatment returned
thrombosis clotting times to that of control mice (P=0.69). These
findings demonstrate that sustained skin-specific inflammation
promotes aortic root inflammation and thrombosis and suggest that
aggressive treatment of skin inflammation may attenuate pro-
inflammatory and pro-thrombotic pathways that produce cardiovascular
disease in psoriasis patients.Journal of Investigative Dermatology
advance online publication, 10 May 2012; doi:10.1038/jid.2012.112.
PMID: 22572815
And going back to...
Tie it to tie2 and don't DIE (cardio event like the widow maker?)
while doing it please?
OK... stop the infernal pressure... your killing me... already... LoL
http://www.ncbi.nlm.nih.gov/pubmed/19342373
Am J Pathol. 2009 Apr;174(4):1443-58.
Keratinocyte but not endothelial cell-specific overexpression of Tie2
leads to the development of psoriasis.
Wolfram JA, Diaconu D, Hatala DA, Rastegar J, Knutsen DA, Lowther A,
Askew D, Gilliam AC, McCormick TS, Ward NL.
Source
Case Western Reserve University, Department of Dermatology, 10900
Euclid Ave, Cleveland, OH 44106, USA.
Abstract
Psoriasis is initiated and maintained through a multifaceted interplay
between keratinocytes, blood vessels, gene expression, and the immune
system. One previous psoriasis model demonstrated that overexpression
of the angiopoietin receptor Tie2 in endothelial cells and
keratinocytes led to the development of a psoriasiform phenotype;
however, the etiological significance of overexpression in each cell
type alone was unclear. We have now engineered two new mouse models
whereby Tie2 expression is confined to either endothelial cells or
keratinocytes. Both lines of mice have significant increases in dermal
vasculature but only the KC-Tie2-overexpressing mice developed a
cutaneous psoriasiform phenotype. These mice spontaneously developed
characteristic hallmarks of human psoriasis, including extensive
acanthosis, increases in dermal CD4(+) T cells, infiltrating epidermal
CD8(+) T cells, dermal dendritic cells and macrophages, and increased
expression of cytokines and chemokines associated with psoriasis,
including interferon-gamma, tumor necrosis factor-alpha, and
interleukins 1alpha, 6, 12, 22, 23, and 17. Host-defense molecules,
cathelicidin, beta-defensin, and S100A8/A9, were also up-regulated in
the hyperproliferative skin. All of the phenotypic traits were
completely reversed without any scarring following repression of the
transgene and were significantly improved following treatment with the
anti-psoriasis systemic therapeutic, cyclosporin A. Therefore,
confining Tie2 overexpression solely to keratinocytes results in a
mouse model that meets the clinical, histological, immunophenotypic,
biochemical, and pharmacological criteria required for an animal model
of human psoriasis.
PMID: 19342373
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19342373/?tool=pubmed
OK so let's see it from 2009 in the P NG?
OK
one hit -
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=PMID%3A+19342373+&start=0&
to
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/d4c7bb61be46d9e/343a42bc8a920114?hl=en&lnk=gst&q=tie2#343a42bc8a920114
And several-- tie2 hits:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=tie2&start=0&hl=en&
And the first tie hit is this pmid: (but we didn't have the pmid # but
did have the abstract)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/d4c7bb61be46d9e/343a42bc8a920114?hl=en&lnk=gst&q=tie2#343a42bc8a920114
OK so PMID: 19342373 made a big stir and the pmid # came out a day or
two later:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/3e764f9d50e3d1d7
And now we've tied PMID: 22572815 to PMID: 19342373 from 2009.
Nice.... so i can stop having my widow maker and make some wise
observations, already...LOL
And ward's #2 of 52 is tie2 in a mouse model with botulinum.
let's see:
http://www.ncbi.nlm.nih.gov/pubmed/22418873
J Invest Dermatol. 2012 Mar 15. doi: 10.1038/jid.2012.60.
Botulinum Neurotoxin A Decreases Infiltrating Cutaneous Lymphocytes
and Improves Acanthosis in the KC-Tie2 Mouse Model.
Ward NL, Kavlick KD, Diaconu D, Dawes SM, Michaels KA, Gilbert E.
Source
1] Department of Dermatology, Case Western Reserve University,
Cleveland, Ohio, USA [2] Department of Neurosciences, Case Western
Reserve University, Cleveland, Ohio, USA [3] The Murdough Family
Center for Psoriasis, University Hospitals Case Medical Center,
Cleveland, Ohio, USA.
PMID: 22418873
This one from this year has psor meat in it... or i'll find it..
http://www.ncbi.nlm.nih.gov/pubmed/22295141
Int J Clin Exp Pathol. 2012;5(1):1-11. Epub 2012 Jan 1.
Transgenic overexpression of keratinocyte-specific VEGF and Ang1 in
combination promotes wound healing under nondiabetic but not diabetic
conditions.
Loyd CM, Diaconu D, Fu W, Adams GN, Brandt E, Knutsen DA, Wolfram JA,
McCormick TS, Ward NL.
Source
Department of Dermatology, Case Western Reserve University Cleveland,
OH 44106, USA.
Abstract
VEGF and Angiopoietin (Ang)1 are growth factors that independently
improve wound healing outcomes. Using a tet-repressible mouse model
coupled with streptozotocin-induced diabetes, we examined wound
healing in diabetic and nondiabetic mice engineered to overexpress
keratinocyte-specific (K5) VEGF, Ang1 or Ang1-VEGF combined. All
nondiabetic mice healed more rapidly than their diabetic counterparts;
however overexpression of VEGF, Ang1 or the combination failed to
improve wound closure under diabetic conditions. Conversely, under
nondiabetic conditions, combining Ang1 and VEGF resulted in rapid
wound closure. Molecular analyses of diabetic and nondiabetic K5-Ang1-
VEGF skin revealed no differences in VEGF expression but an 80%
decrease in Ang1 under diabetic conditions, suggesting an integral
role for Ang1. Nondiabetic K5-Ang1 mice healed more quickly and had
significant increases in granulation tissue and a 60% decrease in re-
epithelialization 7 days after wounding. Furthermore, Ang1 stimulated
primary mouse keratinocytes showed significantly less migration into a
wound bed in an in vitro wound healing bioassay and had decreased
pMAPK, pNFκB, pAkt, and pStat3 signaling. These data suggest that
combined Ang1-VEGF overexpression cannot overcome diabetes-induced
delays in wound healing but is efficacious under nondiabetic
conditions possibly via Ang1-mediated delays in re-epithelialization
and enhancement of granulation tissue formation, thereby allowing more
rapid secondary intention healing.
PMID: 22295141
Free PMC Article
176 hits for: psoria* + vegf -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20vegf
2 of 176 also have ANG1
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20vegf%20ang1
But the first one shows ANG2
And we still get : 2 hits: ang2 + psoria* + vegf -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20vegf%20ang2
==============
http://medicalxpress.com/news/2012-05-vitamin-k2-parkinson-patients.html
Vitamin K2: New hope for Parkinson's patients?
May 11, 2012 in Parkinson's & Movement disorders
Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven,
succeeded in undoing the effect of one of the genetic defects that
leads to Parkinson's using vitamin K2. His discovery gives hope to
Parkinson's patients. This research was done in collaboration with
colleagues from Northern Illinois University (US) and will be
published this evening on the website of the authorative journal
Science.
"It appears from our research that administering vitamin K2 could
possibly help patients with Parkinson's. However, more work needs to
be done to understand this better," says Patrik Verstreken.
Malfunctioning power plants are at the basis of Parkinson's.
If we looked at cells as small factories, then mitochondria would be
the power plants responsible for supplying the energy for their
operation. They generate this energy by transporting electrons. In
Parkinson's patients, the activity of mitochondria and the transport
of electrons have been disrupted, resulting in the mitochondria no
longer producing sufficient energy for the cell. This has major
consequences as the cells in certain parts of the brain will start
dying off, disrupting communication between neurons. The results are
the typical symptoms of Parkinson's: lack of movement (akinesia),
tremors and muscle stiffness.
The exact cause of this neurodegenerative disease is not known. In
recent years, however, scientists have been able to describe several
genetic defects (mutations) found in Parkinson's patients, including
the so-called PINK1 and Parkin mutations, which both lead to reduced
mitochondrial activity. By studying these mutations, scientists hope
to unravel the mechanisms underlying the disease process.
Paralyzed fruit flies
Fruit flies (Drosophila) are frequently used in lab experiments
because of their short life spans and breeding cycles, among other
things. Within two weeks of her emergence, every female is able to
produce hundreds of offspring. By genetically modifying fruitflies,
scientists can study the function of certain genes and proteins.
Patrik Verstreken and his team used fruitflies with a genetic defect
in PINK1 or Parkin that is similar to the one associated with
Parkinson's. They found that the flies with a PINK1 or Parkin mutation
lost their ability to fly.
Upon closer examination, they discovered that the mitochondria in
these flies were defective, just as in Parkinson's patients. Because
of this they generated less intracellular energy – energy the insects
needed to fly. When the flies were given vitamin K2, the energy
production in their mitochondria was restored and the insects' ability
to fly improved. The researchers were also able to determine that the
energy production was restored because the vitamin K2 had improved
electron transport in the mitochondria. This in turn led to improved
energy production.
Conclusion
Vitamin K2 plays a role in the energy production of defective
mitochondria. Because defective mitochondria are also found in
Parkinson's patients with a PINK1 or Parkin mutation, vitamin K2
potentially offers hope for a new treatment for Parkinson's.
<snip>
LOOK go buy some Miso and EAT it... or greens... full of k2... it's
GOOD for YOU..
and might stop that heart attack... i eat the miso with a spoon when
i'm to lazy to put it in hot O2.
======================
C/EBP alpha needed to prevent skin cancer:
http://en.wikipedia.org/wiki/CEBPA
Symbols CEBPA; C/EBP-alpha; CEBP
CCAAT/enhancer-binding protein alpha is a protein that in humans is
encoded by the CEBPA gene.[1][2] The protein encoded by this
intronless gene is a bZIP transcription factor which can bind as a
homodimer to certain promoters and enhancers. It can also form
heterodimers with the related proteins CEBP-beta and CEBP-gamma. The
encoded protein has been shown to bind to the promoter and modulate
the expression of the gene encoding leptin, a protein that plays an
important role in body weight homeostasis. Also, the encoded protein
can interact with CDK2 and CDK4, thereby inhibiting these kinases and
causing growth arrest in cultured cells.[3]
Interactions
CEBPA has been shown to interact with Cyclin-dependent kinase 2[4] and
Cyclin-dependent kinase 4.[4]
<snip>
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/dcdd406a7091e423/2565c88a3d2b6e66?lnk=gst&q=CEBPa#2565c88a3d2b6e66
[...] http://www.medicalnewstoday.com/articles/185087.php
The Rewiring Of Gene Regulation Across 300 Million Years Of Evolution
As published in Science, researchers from Cambridge, Glasgow and
Greece have discovered a remarkable amount of plasticity in how
transcription factors, the proteins that bind to DNA to control the
activation of genes, maintain their function over large evolutionary
distances.
The text books tell us that transcription factors recognise the genes
that they regulate by binding to short, sequence-specific lengths of
DNA upstream or downstream of their target genes. It was widely
assumed that, like the sequences of the genes themselves, these
transcription factor binding sites would be highly conserved
throughout evolution. However, this turns out not to be the case in
mammals.
The authors traced the evolution of gene regulation by comparing the
binding of evolutionarily conserved transcription factors in the
genomes of five vertebrate species - human, dog, mouse, short-tailed
opossum and chicken - spanning 300 million years.
In all tested species, the transcription factors CEBPA and HNF4A are
master regulators of liver-specific genes. By mapping the binding of
CEBPA and HNF4A in the genomes of each species and comparing those
maps, they found that in most cases neither the site nor the sequence
of the transcription factor binding sites is conserved, yet despite
this, these transcription factors still manage to regulate the
largely
conserved gene expression and function of liver tissue.
<sniP>
Is there any latest news on it?
checking:
http://medicalxpress.com/latest-news/
NOPE : this is old news:
http://medicalxpress.com/news/2011-05-lack-gatekeeper-protein-linked-skin.html
Lack of 'gatekeeper' protein linked to skin cancer
May 18, 2011 in Cancer
New research from North Carolina State University shows that a
"gatekeeper" protein plays an important role in skin-cancer prevention
in humans and lab mice.
The protein, C/EBP alpha, is normally abundantly expressed to help
protect skin cells from DNA damage when humans are exposed to
sunlight. The NC State research shows, however, that the protein is
not expressed when certain human skin cancers are present.
Moreover, when the protein is inactivated in special lab mice exposed
to small amounts of the UVB solar radiation, the mice become more
susceptible to skin cancer.
Dr. Robert Smart, professor of environmental and molecular toxicology
at NC State and the corresponding author of a paper in the Journal of
Investigative Dermatology describing the research, says that C/EBP
alpha serves as an important "pause button" in cells. If there is any
DNA damage, C/EBP alpha halts the cell-replication process to allow
time for cells to repair themselves to prevent DNA errors from
occurring.
"Loss of C/EBP alpha expression is associated with some of the most
common human cancers, including breast and colon cancer," Smart says.
"We think it may also have a role in tumor suppression in these
cancers via its gatekeeper function."
In the study, the researchers found that human skin expresses C/EBP
alpha as does the pre-cancerous, benign lesion called actinic keratose
– the precursor to skin cancer.
"C/EBP alpha is expressed in normal human skin and in pre-cancerous
actinic keratoses, but something happens when cancerous lesions appear
– the protein is not expressed," Smart says. "We then asked, 'Is the
loss of C/EBP alpha contributing to tumor formation?' The answer seems
to be yes."
Smart and colleagues exposed hairless, genetically modified mice –
bred with C/EBP alpha inactivated – to low doses of the UVB solar
radiation. The mice were highly susceptible to certain common types of
skin cancer – squamous cell carcinomas – with these cancerous tumors
developing and growing rapidly.
"If you can figure out how to keep C/EBP alpha turned on, maybe the
tumor would stay in its pre-cancerous state," Smart says.
Smart adds that figuring out how the protein fulfills its gatekeeper
role – and how and why the protein is inactivated in cancerous cells –
marks the next step in his research.
More information: "C/EBP alpha Expression is Downregulated in Human
Nonmelanoma Skin Cancers and Inactivation of C/EBP alpha Confers
Susceptibility to UVB-Induced Skin Squamous Cell Carcinomas" Elizabeth
A. Thompson, et al. Published: June 2011 print edition of Journal of
Investigative Dermatology
Abstract
Human epidermis is routinely subjected to DNA damage induced by UVB
solar radiation. Cell culture studies have revealed an unexpected role
for C/EBP alpha (CCAAT/enhancer-binding protein-alpha) in the DNA
damage response network, where C/EBP alpha is induced following UVB
DNA damage, regulates the G1 checkpoint, and diminished or ablated
expression of C/EBP alpha results in G1 checkpoint failure. In the
current study we observed that C/EBP alpha is induced in normal human
epidermal keratinocytes and in the epidermis of human subjects exposed
to UVB radiation. The analysis of human skin precancerous and
cancerous lesions (47 cases) for C/EBP alpha expression was conducted.
Actinic keratoses, a precancerous benign skin growth and precursor to
squamous cell carcinoma (SCC), expressed levels of C/EBP alpha similar
to normal epidermis. Strikingly, all invasive SCCs no longer expressed
detectable levels of C/EBP alpha. To determine the significance of C/
EBP alpha in UVB-induced skin cancer, SKH-1 mice lacking epidermal C/
EBP alpha (CKO alpha) were exposed to UVB. CKO alpha mice were highly
susceptible to UVB-induced SCCs and exhibited accelerated tumor
progression. CKO alpha mice displayed keratinocyte cell cycle
checkpoint failure in vivo in response to UVB that was characterized
by abnormal entry of keratinocytes into S phase. Our results
demonstrate that C/EBP alpha is silenced in human SCC and loss of C/
EBP alpha confers susceptibility to UVB-induced skin SCCs involving
defective cell cycle arrest in response to UVB.
===============
St john's wort:
http://www.ncbi.nlm.nih.gov/pubmed/22571563
Australas J Dermatol. 2012 May;53(2):131-5. doi: 10.1111/j.
1440-0960.2012.00877.x. Epub 2012 Mar 8.
The evaluation of the clinical effect of topical St Johns wort
(Hypericum perforatum L.) in plaque type psoriasis vulgaris: A pilot
study.
Najafizadeh P, Hashemian F, Mansouri P, Farshi S, Surmaghi MS,
Chalangari R.
Source
Department of Pharmacology, Pharmaceutical Sciences Branch, Islamic
Azad University Department of Clinical Pharmacy, Pharmaceutical
Sciences Branch, Islamic Azad University Department of Dermatology,
Imam Hospital, Tehran University of Medical Sciences Skin and Stem
Cell Research Center Department of Pharmacognosy, Faculty of Pharmacy,
Tehran University of Medical Sciences, Tehran, Iran.
Abstract
In this case series, ten patients with plaque-type psoriasis were
treated with Hypericum perforatum ointment. The hypericum ointment was
applied to one side of each patient's body and the vehicle to the
opposite side twice daily for 4 weeks in a single blinded manner.
Modified psoriasis area severity index (PASI) scores were
significantly lowered where the formulated ointment had been applied.
In determining PASI scores, three factors, erythema, scaling and
thickness, were evaluated; all were significantly lower where the
formulated ointment had been applied (P = 0.01, P = 0.004, P = 0.04).
Hypericum perforatum ointment applied twice daily may be effective in
reducing PASI scores in mild plaque-type psoriasis, however, further
larger studies need be conducted to achieve a more conclusive result.
PMID: 22571563
115 hits: john's wort - p ng
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=+john%27s+wort&start=0&hl=en&
17 hits: Hypericum
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=Hypericum+&start=0&hl=en&
Hypericum perforatum - 9 hits - p ng:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=Hypericum+perforatum+&start=0&hl=en&
And i've got some good info in this THREAD:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/c51c599ee125d14a/76469b4a2421d541?hl=en&lnk=gst&q=Hypericum+perforatum+#76469b4a2421d541
OK i've got to GO WATCH my Nephews BASEBALL game...s
I hope i don't have ONE of these cardio BAD days... not like bad hair
days..LOL.... taking some fish oils..... next... LOL
http://en.wikipedia.org/wiki/Widow_maker
A widow maker is a nickname used to describe a highly stenotic left
main coronary artery or proximal left anterior descending coronary
artery of the heart.
This term is used because if the artery gets abruptly and completely
occluded it will cause a massive heart attack that will likely lead to
a sudden death. The blockage that kills is made up of platelets
streaming to the site of a ruptured cholesterol plaque. Even a small
amount of plaque in this area can (for a variety of poorly understood
reasons) rupture and cause death; bypassing chronic blockages or
trying to open them up with angioplasty does not prevent heart attack
but it can restore blood flow in case of a sudden blockage or heart
attack. An example of the devastating results of a complete occlusion
of the LAD (Left Anterior Descending) artery was the sudden death of
former NBC News Washington Bureau Chief Tim Russert.
From the minute a widow maker hits, survival time ranges from minutes
to several hours. Rapidly progressing symptoms should signal need for
immediate attention. Symptoms of initial onset may include nausea,
shortness of breath, pain in the head, jaw, arms or chest, often of a
novel but imprecise sensation which builds with irregular heart beat.
Early symptoms may be mistaken for food poisoning, flu or general
malaise until they intensify. A widow maker cannot kill
instantaneously but induce cardiac arrest which may do so within 10 to
20 minutes of no circulation. A victim with no pulse or breath is
still alive living off oxygen stored in the blood and may be able to
be rescued if treatment is begun promptly within this window. [1].
<snip>
Did Russert have some fish oil in his diet?
What's that other stuff i say to take... i took ONE and i'm in the
PINK today..
Oh yeah... 5HTP from africa.. the little black
http://en.wikipedia.org/wiki/Griffonia_simplicifolia
Griffonia simplicifolia (syn. Bandeiraea simplicifolia Benth.) is a
woody climbing shrub native to West Africa and Central Africa. It
grows to about 3 m, and bears greenish flowers followed by black pods.
Chemical constituents
The seeds of the plant are used as an herbal supplement for their 5-
hydroxytryptophan (5-HTP ) content.[2][3] 5-Hydroxytryptophan is an
important building block for the human body to form serotonin.[4]
Serotonin plays an important role in the body specially as a
neurotransmitter to transport signals between neurons in the nervous
system. Griffonia simplicifolia also has a legume lectin called GS
Isolectin B4, which binds to alpha-D-galactosyl residues of
polysaccharides and glycoproteins.
<snip.>
I'm gonna take two of these dudes... i'm feeling xlnt.
randall... living large and getting UVB's from the sun = D3 in ME...
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